okay so i was going through this document trying to put arrows of what i rememered, and guess what, THIS

IS THE SHELF I JUST TOOK! lol so i got tired of putting arrows b/c every SINGLE one of these questions is on it, most of them are verbatim (just CHECK THE ANSWERS by urself before taking the shelf) but this is the ONLY le you need for neuro shelf people!

Brainstorm 2010

1. Hows does CSF enter the subarachnoid space? -Subarachnoid granulations -Subarachnoid granulations (this is how CSF ows from the subarachnoid space into the dural venous sinuses, if it asks how it ENTERS the subarachnoid space, its through the fourth ventricle and Foramina Luschka/ Foramen of Magendie). The CSF ows from the subarachnoid space into the dural venous sinuses through arachnoid villi, but the blood from the dural venous sinuses cannot ow back into the subarachnoid space via these villi. Normally, the pressure in the subarachnoid space is greater (about 200 mm H2O) than that in the dural venous sinuses (about 80 mm H2O); this pressure difference promotes the CSF ow into the dural venous sinuses through the ne tubules located in the arachnoid villi. However, even if the pressure in the dural venous sinuses exceeds that of the subarachnoid space, the blood from the dural sinuses does not ow back into the subarachnoid space because the tubules in the arachnoid villi collapse. ! The fourth ventricle communicates with the subarachnoid space via two lateral apertures, called the!foramina of Luschka, and one medial aperture, the!foramen of Magendie!(Fig. 3-3A). Circulation The movement of CSF is pulsatile. It ows from the lateral ventricles into the third ventricle through the foramina of Monro (Fig. 3-3A; the direction of ow is indicated by arrows) where it mixes with more CSF. Then, it ows through the cerebral aqueduct (aqueduct of Sylvius) into the fourth ventricle, where additional CSF is secreted. The uid leaves the ventricular system via the foramina of Luschka and Magendie and enters the cerebellomedullary cistern (cisterna magna). The CSF then travels rostrally over the cerebral hemisphere where it enters the arachnoid villi (Fig. 3-1A). The arachnoid villi allow ow of CSF into the dural venous sinuses but do not allow ow in the opposite direction because the pressure in the subarachnoid space is higher (about 200 mm H2O) compared with the pressure in the dural venous sinuses (about 80 mm H2O). The CSF in the cerebellomedullary cistern also ows downward into the spinal subarachnoid space and then ascends along the ventral surface of the spinal cord into the basal part of the brain where it courses dorsally to empty into the dural sinuses (Fig. 3-1A). ! 2. A baby is born with a congenital disorder that causes him to have no!unmyelinated!bers. What type of loss does this causes? -Pain (Answer? please check) -Joint propioception -Motor function -Vibration -Pressure! Pain Afferents Pain afferents can be!myelinated!or!unmyelinated.
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glutamate receptors and NMDA

!!!!!!!!!The myelinated pain afferents belong to the class of afferent axons termed the!Adelta bers!and conduct action potentials between about 5 to 30 meters/sec. These are the smallest and slowest of the myelinated axons. (By contrast, myelinated axons for ne touch and proprioception conduct at about 35 to 120 meters/sec.) !!!!!!!!!The unmyelinated pain bers belong to the class of afferent bers called the!C bers!and conduct from about 0.4 to 1.0 meters/secon An A-delta ber responds to either mechanical stimuli or temperature stimuli in the painful realm and produces the acute sensation of sharp, bright pain. Their neurotransmitter in the dorsal horn is!glutamate!acting on AMPA receptors. By contrast, a C ber can respond to a broad range of painful stimuli, including mechanical, thermal or metabolic factors. The pain produced is slow, burning, and long lasting. The neurotranmitter in the dorsal horn is!glutamate!along with certain peptides such as!substance P. The receptors for glutamate are not only AMPA, but also!NMDA. Since the latter only open following!prolonged depolarization, continual stimulation of C bers eventually causes greater excitation in the postsynaptic neurons in the dorsal horn as the NMDA receptors start added to the response. The receptor for capsaicin, which is found in hot peppers, is located in the C bers. This ion channel normally is opened by hot stimuli. http://courses.washington.edu/conj/sensory/pain.htm

5. Pt presents with problems in the R conjugate gaze while the L conjugate gaze is intact. Movement of the head towards the R causes both eyes to rst move to the left and then to the R. Where is the lesion? !!!!!!!!!!!!!!!!a. Frontal !!!!!!!!!!!!!!!!b. insular !!!!!!!!!!!!!!!!c. parietal !!!!!!!!!!!!!!!!d. temporal !!!!!!!!!!!!!!!!e. occipital (A) Several of the key relationships revealing the connections between the cerebral cortex and the pontine gaze center as well as the linkage between CN VI and III are shown. Concerning conscious regulation of conjugate gaze, this process originates from the frontal lobe, where axons project to the contralateral horizontal gaze center (1). In this manner, activation of the left frontal eye eld will result in movement of the eyes to the right because of excitation of the right abducens and left oculomotor nucleus. Briey, the major structure for the integration!and control of horizontal gaze is the pontine gaze center. It receives inputs from the contralateral cerebral cortex and ipsilateral vestibular nuclei. After integrating signals from these regions, the pontine gaze center projects its axons to the nucleus of CN VI on the ipsilateral side and the nucleus of CN III on the contralateral side. In this manner, stimulation of the right pontine gaze center by either the ipsilateral vestibular nuclei or contralateral cerebral cortex will result in activation of the ipsilateral CN VI and the contralateral CN III. The effects of stimulation will thus cause the right eye to be abducted and the left eye to adduct (i.e., the eyes are directed to the right). Conversely, if there is a lesion of the right pontine gaze center, then the eyes cannot be moved to the right. However, the left pontine gaze center, which remains intact, allows the eyes to be moved to the left. Testing of the horizontal eye movement reex is done by passively turning the head from side to side, and if the reex is intact, the eyes will move conjugately in the direction opposite to movement. Horizontal Gaze Palsy:!The most common cause is damage to the brain stem, often by a stroke. Often, the palsy is complete and severe. That is, the eyes cannot move to the side at all. Palsies can also be caused by damage to the!front part of the cerebrum, usually by a stroke. The resulting palsy
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may not be as severe as that caused by damage to the brain stem, and symptoms often lessen with time. Milder palsies may cause only nystagmus or inability to maintain xation. http://dstrong.blog.uvm.edu/neuroblog/conjugate%20gaze.jpg To consciously direct horizontal eye movements, bres from the cortex (supplementary/premotor) project to the horizontal gaze center (aka ParaPontine Reticular Formation, PPRF). If these cortical bres are lesioned, then you cannot initiate that eye movement. 6. A 35 yr old female presents with a 3-month history of amenorrhea and progressive bitemporal hemianopia, which occurred rst in the upper visual eld. Wheres the lesion thats causing this defect of the visual eld? " a. maligdenoma? at infundibular silla turcica " b. Pituitary adenoma " c. neoplasm at cavernous sinus " d. neoplasm at temporal retinal bers, bitemporal " e. sacular aneurysm of circle of willis Bitemporal hemianopsia (Bitemporal hemianopia) is a type of partial blindness where vision is missing in the outer half (temporal) of both the right and left visual eld. It is usually associated with lesions of the optic chiasm, the area where the optic nerves from the right and left eyes cross near the pituitary gland. Bitemporal hemianopsia most commonly occurs as a result of tumors located at the mid-optic chiasm. Since the adjacent structure is the pituitary gland, some common tumors causing compression are Pituitary adenomas, and Craniopharyngiomas. Also another relatively common neoplastic etiology is Meningiomas. Paris as seen with bitemporal hemianopsia Pituitary tumors Neoplasms involving the pituitary gland, hypothalamus, or both most commonly give rise to loss of function, often with systemic metabolic or endocrinologic effects. Combinations of loss of posterior pituitary function (diabetes insipidus) and anterior pituitary function (hypogonadism, hypoadrenalism, hypothyroidism, and insufcient growth) may be seen. Hypothalamic involvement may also cause changes in behavior (hypophagia, hyperphagia, placidity, sedation, low threshold for rage reactions) and autonomic function disorders (Horner's syndrome, disordered temperature regulation with hypothermia from posterior involvement or hyperthermia from anterior involvement). Encroachment on the neighboring optic chiasm leads to visual eld defects,!classically bitemporal hemianopia!(see!Chap. 3). This can also be seen with craniopharyngioma, a benign, cystic tumor that derives from remnants of Rathke's pouch. Anterior pituitary tumors may produce positive humoral effects via increased secretion of pituitary hormones. Eosinophilic adenomas secreting growth hormone are associated with gigantism in children or acromegaly in adults, whereas basophilic adenomas are associated with Cushing's hyperadrenal syndrome. Anterior pituitary adenomas are frequently associated with excess prolactin production and galactorrhea (often accompanies by amenorrhea and infertility). http://www.dartmouth.edu/~dons/part_3/ chapter_28.html#chapter_28_pituitary_tumors
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7) Paciente inconsciente por 4 horas. No responde a comandos verbales, pero sus piernas y brazos si responden a estimulos dolorosos moviendose. Sus pupilas estan dilatadas 3-4mm, responden a la luz adecuadamente. Cuando le hacen la prueba del conjugate gaze y sale normal Tiene respiracin normal sin ayuda de ventilador. Pregunta que esta daado o funcionando. Te ponen una tablita:! Midbrain-Pons-Medulla, con diferentes combianciones entre daado y funcionando y eliges la combinacin correcta. What are the consequences of lesions of the reticular formation? From the earlier discussion, it is not surprising that lesions of the brainstem reticular formation are associated with disturbances of consciousness. Damage (typically associated with a cerebrovascular accident) to the reticular formation of the pons or midbrain will produce!coma!in most instances. The electroencephalographic patterns resulting from lesions of different regions of the reticular formation may vary signicantly. For example, lesions of the midbrain reticular formation result in the appearance of slow waves of large amplitude. In contrast, lesions of the pons are frequently characterized by an alpha rhythm typically seen in a normal drowsy person. With other lesions, the patient may display an EEG pattern characteristic of slow-wave sleep.!In the case of a pontine lesion, the patient lies quietly and displays a variety of autonomic and somatomotor reexes as well as normal eye movements.!This constellation of responses is referred to as!coma vigil!or!akinetic mutism. Lesions involving the lower brainstem also produce a loss of consciousness. However, lesions involving the lower brainstem are frequently fatal because of the severity of the accompanying cardiovascular respiratory disturbances. (Siegel and Sapru) Response to noxious stimuli: - With damage to the diencephalon decorticate posturing may be seen following noxious stimulation (see Fig.!8-1). Decorticate posturing includes exion of the arm, wrist and ngers, with extension of the lower limbs. This posturing may be asymetrical initially (appearing rst on the more damaged side). -With damage to the mesencephalon or upper pons, decerebrate posturing begins to appear following noxious stimulation. This consists of extension and internal rotation of the arms and legs (see Fig.!8-1). -Damage to the lower pons and medulla eliminates the response to noxious stimuli. Acute cross-sectional loss of the lower pons almost invariably results in accid quadriplegia Pupil Response: -Isolated damage or suppression of the cerebral cortex will not change the pupil or its reexes. -However, if the pons or medulla is selectively involved (with preservation of midbrain function) the pupils will be small and reactive because only the descending sympathetic pathways are damaged -If the diencephalon is severely damaged the pupils are constricted due to suppression of the hypothalamic origins of the sympathetic pupillodilator system. However, they will still react to light. Conjugate gaze: -Diffuse cerebral cortical damage or suppression of cortical function results in loss of the fast component of the vestibulo-ocular reex. The degree of suppression of this fast component is proportional to the degree of suppression/damage. Tonic conjugate horizontal deviation of the eyes during caloric or oculocepahlic testing indicates preserved brain stem reex activity (and, by extension, intact reticular activating system) with loss of cortical input.
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-Damage to the mesencephalon produces loss of medial rectus response to caloric and oculocephalic stimulation, with intact lateral rectus function. The corneal reex will be preserved since this is mediated at the pontine level. -With brain stem damage through the lower pons there is loss of all response to caloric and oculocephalic stimulation because the paramedian reticular formation subserving conjugate horizontal gaze and the sixth-nerve nuclei are affected. At this stage there will be no corneal reex http://www.dartmouth.edu/~dons/part_2/chapter_17.html 8) Paciente con narcolepsy que tambien tiene cataplexia. Dice que rapido que le dan sus ataques de narcolepsia comienza a soar En que fase del sueo se encuentra (La pregunta no dice de forma explicita que es narcolepsia y cataplexia, te da los sintomas y uno lo deduce): !!!!!!!!!!!!!!!!!!!!!!!!!! -REM- esta fue mi contestacin! !!!!!!!!!!!!!!!!!!!!!!!!!! -Non rem 1 !!!!!!!!!!!!!!!!!!!!!!!!!! -Non rem 2 !!!!!!!!!!!!!!!!!!!!!!!!!! -Non rem 3 !!!!!!!!!!!!!!!!!!!!!!!!!! -Non rem 4 The loss of muscle tone during a cataplectic episode resembles the interruption of muscle activity that naturally occurs during REM sleep. A group of neurons in the brainstem ceases activity during REM sleep, inhibiting muscle movement. Using an animal model, scientists have recently learned that this same group of neurons becomes inactive during cataplectic attacks, a discovery that provides a clue to at least one of the neurological abnormalities contributing to human narcoleptic symptoms. http://www.ninds.nih.gov/disorders/narcolepsy/detail_narcolepsy.htm 9. Pt with (describtion of Broca's aphasia), what other motor problems you are likely to see? -> Contralateral weakness of lower face and arm. --------------------------------------------------------------+ La contestacion exacta creo que es: Paresis of right lower face and arm. Frontal Lobe (Broca's Area) A different form of aphasia called motor or nonuent aphasia results from a lesion of the posterior aspect of the inferior frontal gyrus (called Broca's area). In motor aphasia, the patient is unable to express ideas in spoken words. With respect to both receptive and motor forms of aphasia, two points should be noted. The rst is that it is likely that Broca's area and Wernicke's area are functionally interrelated because they can communicate with each other through a pathway referred to as the arcuate fasciculus (Fig. 26-18). The second point is that both forms of aphasia occur only when the dominant hemisphere is affected (see discussion on pages 487#490 concerning cerebral dominance). Lesions of the Motor Regions of the Frontal Lobe In brief, a moderate to large lesion of the motor cortex will produce an upper motor neuron paralysis (as opposed to a discrete lesion of motor cortex, which has been reported to produce a accid paralysis). The upper motor neuron paralysis is characterized by a paralysis of thecontralateral limb(s),!hyperreexia, hypertonia, and a Babinski sign. A lesion of parts of area 6 will produce apraxia, which is the inability to carry out certain types of complex learned movements (see discussion in Chapter 19). It is presumably due to the loss of the programming mechanism for the
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execution of movements. A lesion of the posterior aspect of the inferior frontal cortex (Broca's area) will produce expressive or motor (nonuent) aphasia. As noted previously, this disorder is characterized by difculty in expressing ideas in a meaningful manner. (Siegel and Sapru) A type of non-uent aphasia is Brocas aphasia. People with Brocas aphasia have damage to the frontal lobe of the brain. They frequently speak in short phrases that make sense but are produced with great effort. They often omit small words such as is, and, and the. For example, a person with Brocas aphasia may say, Walk dog, meaning, I will take the dog for a walk, or book book two table, for There are two books on the table. People with Brocas aphasia typically understand the speech of others fairly well. Because of this, they are often aware of their difculties and can become easily frustrated.!People with Brocas aphasia often have right-sided weakness or paralysis of the arm and leg because the frontal lobe is also important for motor movements. http://www.nidcd.nih.gov/health/voice/aphasia.asp 10.La 10 eran muchos sintomas que eran de una enfermedad autoimune, solo te decian los sintomas y no la enfermedad. Tenias que discriminar si era del CNS o PNS para decir en que celulas ocurre demyelination....! CNS - Olygodendrocites PNS - Schwan cells Demyelinating disease of the PNS=!GBS (Guillain-Barre) is a dramatic acute demyelinating neuropathy with rapid onset (hours to days). This usually produces weakness of the extremities and axial musculature, which can evolve to respiratory motor failure and asphyxiation if support is not available. Autonomic involvement may lead to threatening blood pressure irregularities and cardiac arrhythmias. This condition often involves the largest sensory nerve bers as well. Because the largest, most heavily myelinated sensory bers are the muscle stretch bers, and since these bers and the motor axons are direct parts of the reex arc, deep tendon reexes are almost always lost very early in the course of the condition, even in muscles that are not yet clinically weak. As the condition progresses, there can be sensory change, as well (usually numbness and tingling), but the picture is usually dominated by accid weakness. Although the most common presentation is with an ascending paralysis, rarely, it can begin by affecting cranial muscles. Diagnosis can be aided by CSF evaluation, which shows high protein levels, with very few actual inammatory cells (usually not above the upper limit of normal). This has been termed "cytoalbuminologic dissociation." Demyelinating disease of the CNS= Multiple Sclerosis: Lesions in the optic nerve produce optic neuritis. If the plaque involves the optic disk, edema is seen on funduscopic examination (optic papillitis); if it involves the nerve behind the disk, there are no acute changes on funduscopic examination (retrobulbar neuritis). In either case, optic atrophy often develops with time, though it is not apparent before about two weeks after the symptomatic onset. Acute optic neuritis is usually associated with pain on eye movements (due to irritation of the optic nerve), and there is some visual eld defect (usually a central or paracentral scotoma). Although 40% of persons with MS have optic neuritis, up to 40% of patients with optic neuritis do not go on to develop MS (some of these may actually have ischemic optic nerve disorders, while others have what has been termed a "clinically isolated syndrome", where symptoms remain in one location).

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The medial longitudinal fasciculus is a tract that is occasionally involved by demyelinating plaque, producing unilateral or bilateral internuclear ophthalmoplegia (see!Chap. 4). During attempted lateral gaze there is paresis of the medial rectus (insufcient adduction) and nystagmus of the abducting eye. However, convergence movement of the medial rectus is usually spared. Internuclear ophthalmoplegia is almost always due to demyelination, but it can rarely be seen in persons with vascular disease (especially the elderly) and very rarely results from tumor in the fourth ventricle or other inammatory conditions. Damage to spinal cord pathways (myelopathy) is yet another common presentation. This can include damage to descending motor pathways, producing spastic hemiparesis or damage to sensory tracts (usually the dorsal columns). In the latter case, paresthesias may be very distressing. The cerebellar connections can be affected with incoordination of the limbs, ataxia and dysarthria (scanning speech or "drunken speech). Tic douloureux (trigeminal neuralgia) sometimes occurs, and MS must be a consideration in a young patient with this presentation. Lhermitte's symptom, an electric or tingling sensation referred to the trunk and limbs during neck exion (chin on chest), was rst described in association with multiple sclerosis. It is presumed to be caused by stretch of damaged dorsal columns, depolarizing axons (see!Chap. 1). Although this can appear with other intrinsic and occasionally extrinsic spinal cord lesions, it is most commonly seen with multiple sclerosis. The vestibular system may result in imbalance, but usually vertigo (if present) is mild, while nystagmus can be severe and bizarre. Certain nonspecic symptoms are quite common, including fatigue. However, it is important to consider alternative explanations for this before ascribing symptoms to this mechanism. http://www.dartmouth.edu/~dons/index.html ! ! 11. Embryonic origin of gamma neurons ? Answers : I was between alar plate and basal plate Motor nerve bers begin to appear in the fourth week, arising from nerve cells in the basal plates (ventral horns) of the spinal cord. These bers collect into bundles known as!ventral nerve roots -Langmans 12. is missing 13. they give a diagram about sleeping patterns. They give you a case about an old lady who has trouble falling asleep and you have to analyze the differences in sleeping patterns with that of younger people!! !!- I think the answer is that the old lady has more awake periods than the others. !Do older individuals have more sleep problems than young people? The commonality of sleep problems among older adults is now well established. Many factors may interfere with optimal sleep and wakefulness in older adults and explain a signicant proportion of this age-related increase in sleep difculties. Acute and chronic illness, the side effects of medication, mental health conditions, primary sleep disorders and abrupt, uncontrollable changes in both social and personal life may all contribute to the development of sleep difculties in the elderly. Older subjects suffer more from primary sleep disorders The prevalence of some primary sleep disorders such as sleep apnea disorder (pauses in breathing during sleep), periodic leg movement in sleep (repetitive limb movements during sleep that may induce partial or complete awakenings), and restless sleep
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syndrome (overwhelming urge to move the legs usually caused by uncomfortable or unpleasant sensations in the legs) starts to increase signicantly in the middle years of life. The National Sleep Foundation estimates that 35% or more of people aged 65 years and older experience periodic leg movement in sleep. Others have estimated that 4% of men and 2% of women over the age of 50 have sleep apnea in addition to experiencing excessive daytime sleepines Sleep changes occur from cradle to grave. Important modications of the sleepwake cycle occur also in optimal aging, i.e., in individuals free of any medical or psychiatric condition, and who do not present with specic sleep disorders. Compared to young subjects, elderly individuals show: 1. Earlier bedtimes and earlier wake-up times 2. More sleep during the day (naps) 3. Less sleep less during the night 4. More awakenings during the sleep episode, especially in the second half of the night. Lighter sleep. Also- we learned in class that you have less REM periods (because you tend to sleep less hours) http://css.to/sleep/sleep_aging.pdf 14. a case about a 10 day old baby who presents with muscle weakness, fever, can't eat... mother takes him to the hospital. He has a healthy 2 year old sister and the mother had lost !a baby previously who died at like 2 weeks of age.... they want to know what was the likely genetic cause.!! one of the answer choices was X-linked muscle dystrophy! From the Muscular dystrophy society of America
Becker Muscular Dystrophy (BMD) !! Onset: Adolescence or adulthood. Symptoms: " Generalized weakness and muscle wasting rst affecting the muscles of the hips, pelvic area, thighs and shoulders.Phosphoglycerate Kinase Deciency !! Onset: Infancy to early adulthood. Symptoms: May cause anemia, enlargement of the spleen, mental retardation and epilepsy (seizures); more rarely, weakness, exercise intolerance, muscle cramps and episodes of myoglobinuria (rust-colored urine indicating breakdown of muscle tissue). Progression: Muscle symptoms slowly progressive. Inheritance: X-linked recessive, mostly affects males, although females are carriers. Calves often are enlarged. BMD is similar to Duchenne muscular dystrophy but often much less severe. There can be signicant heart involvement. Progression: Disease progresses slowly and with variability but can affect all voluntary muscles. Most with BMD survive well into mid-to-late adulthood. Inheritance: X-linked recessive. BMD primarily affects boys, who inherit the disease through their mothers. Women can be carriers of BMD but usually exhibit no symptoms Emery-Dreifuss Muscular Dystrophy (EDMD) Onset: Usually by 10 years of age. Symptoms:
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Weakness and wasting of shoulder, upper arm and calf muscles; joint stiffening; fainting (because of cardiac abnormalities). Progression: Disease usually progresses slowly. Cardiac complications are common and sometimes require a pacemaker. Inheritance: Can be X-linked recessive, primarily affecting males, who inherit the disease through their mothers. Another type is autosomal dominant, meaning it can be inherited through either parent; an autosomal-recessive type occurs when a faulty gene is inherited from each parent.

http://www.mda.org/disease/40list.html 15) 49 year old female patient who gradually lost sensibility in her upper extremities. Answer: Based on the description of the case, the patient suffered from syringomelia. However this was not one of the options, you needed to know the tract that was affected (Spinothalamic ) and that they cross at the white commissure.!! BRS REFERENCE: PG149 is a central cavitation of the cervical spinal cord of unknown etiology. results in destruction of the ventral white commissure and interruption of decussating spinothalamic bers, causing bilateral loss of pain and temperature sensation. can result in extension of the syrinx into the ventral horn, causing an LMN lesion with muscle wasting and hyporeexia. Atrophy of lumbricals and interosseous muscles of the hand is a common nding. can result in extension of the syrinx into the lateral funiculus, affecting the lateral corticospinal tract and resulting in spastic paresis (a UMN lesion). can result in caudal extension of the syrinx into the lateral horn at T1 or lateral extension into the lateral funiculus (interruption of descending autonomic pathways), resulting in Horner syndrome. 16) Patient with ptosis palpebral, anisocoria and anhydrosis on one side of the face. Answer: This is a case of Horner syndrome. Remember symptoms are ipsilateral to the structure that is damage, and the problem is of the sympathetic system. Anatomy BRS Reference pg 360 Horner's syndrome- caused by thyroid carcinoma of cervical sympathetic trunk by Pancoast tumor at apex of lungs, injures stellate ganglion, injury to neck and cervical sympathetic nerves. Causes ptosis,miosis, enopthalmos (sunken eyes),anhidrosis and vasodilation. WIKIPEDIA REFERENCE: Signs found in all patients on affected side of face include; ptosis (which is drooping of the upper eyelid from loss of sympathetic innervation to the superior tarsal muscle, also known as Mller's muscle [1]), upside-down ptosis (slight elevation of the lower lid), and miosis (constricted pupil), and anhidrosis (decreased sweating on the affected side of the face), dilation lag (slow response of the pupil to light), Enophthalmos (the impression that the eye is sunk in) loss of ciliospinal reex and bloodshot conjunctiva may occur
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depending on the site of lesion. Sometimes there is ushing of the face is on the affected side of the face due to dilation of blood vessels under the skin. A guy in an accident that lost his hand at the wrist. He was rushed to the ER and the hand was kept in a saline solution. What will have to happen for the nerves to be restored?! a. The nerves must be viable in the hand! b. The Schwann cells have to grow towards the arm! Neuro Roadmap pg 51 Neurons with severed axons in the PNS are capable of complete axonal regeneration (Fig. 2-9b) 1.successful sprouts from cut axon grow into endoneurial sheathes and are guided by Schwann cells to targets Regeneration proceeds at 1-2mm/day (slow anterograde transport) At target Schwann cells begin myelin production Diameter of regenerated axon is less than original axon, so conduction velocity of nerve impulse is slower Axons in PNS may not regenerate completelys or may grow back to wrong target (synkenesis) i.e. So if there were an option which said Schwann cells grow towards hand/wrist this might be correct 18. What inhibits prolactin? Dopamine RM p.42 Dopamine acts as an inhibitory factor that regulates the release of prolacting. http://edrv.endojournals.org/cgi/content/abstract/22/6/724 Dopamine reaches the pituitary via hypophysial portal blood from several hypothalamic nerve tracts that are regulated by PRL itself, estrogens, and several neuropeptides and neurotransmitters. Dopamine binds to type-2 dopamine receptors that are functionally linked to membrane channels and G proteins and suppresses the high intrinsic secretory activity of the pituitary lactotrophs. In addition to inhibiting PRL release by controlling calcium uxes, dopamine activates several interacting intracellular signaling pathways and suppresses PRL gene expression and lactotroph proliferation. 19-20 missing 21. Know parts of rostral medulla (pg 106-107 Haines).! pointed to pyramidal decussation and ML 22. Know what nerve root is affected in damage of the brachioradilis BRS. p.50 Brachioradialis is innervated by Radial nerve (C5-T1) 23. Know what kind of neurological decits are caused by a lack of Vitamin B12. Couldnt nd it in a book so: !Wikipedia Reference: Early and even fairly pronounced deciency does not always cause distinct or specic symptoms. Common early symptoms are tiredness, a decreased mental work capacity, weakened concentration and memory, and irritability and depression.
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Neurological signs of B12 deciency, which can occur with or without anemia, include sensory disturbances (due to damage to peripheral nerves caused by demyelination) and irreversible nerve cell death. Symptoms include numbness and/or tingling of the extremities, altered proprioception, impaired sense of smell, loss of appetite (anorexia), disturbed coordination and, if not treated in time, an ataxic gait especially in the dark when there is less visual reference. The following symptoms have been recorded, beginning with those perhaps most likely to be indicative of B12 deciency. 1. Itchy or tingling tongue. The tongue suddenly itches from time to time without warning. This occurs on the edge of the tongue, along one side or the other or at the tip. Some individuals experience stinging, pain, or tingling instead of itching. 2. White spots in the skin, resulting from melanin becoming absent in the area. These often occur on the outside of the forearm, but may occur in other places. The longer these spots are there, the whiter they get. As time goes by, the spots become very dry and aky to the extent that small raw spots of skin may be exposed. 3. Sharp stabbing, tingling pain in the palm of one or both hands. This occurs suddenly and for no apparent reason in a spot directly below the ring nger, approximately where the rst palm crease is. If B12 deciency is not treated, a tingling pain may begin to occur along the outside edge of the hand, starting from the wrist. This pain occurs when the wrist is extended. 4. Sores at the corners of the mouth, sometimes extending along the edge of the lip. These are raw spots, not blisters, and they tend to come and go. 5. Nerve shock in the side of the body. It can be felt coming on a few seconds before it hits, and then it hits almost like a mild but deep electric shock and quickly subsides. It can occur at the side of either hip or on either side of the upper body, along the ribs. It can occur consecutively in at least two or three locations, one right after the other. 6. Shortness of breath, but without chest pain. This can occur when walking just a few yards. 7. Hemifacial (one side of the face) spasm usually manifesting in the eye. Can occur in multiple spots on the face such as the lip, nose, eyelids, and eyebrow. 8. Facial pain, usually on only one side of the face at a time. This pain varies so much that it would be difcult to describe all the possibilities. This can present as a dull pain in the cheek bone right underneath an eye, or a sharp shooting pain across the forehead, sometimes coming downward from the scalp to the edge of the nose by the eye. 9. Tingling along the back of one or both thighs, starting at the hips and shooting downward. 10. Memory loss and/or disorientation. 11. Migraine headaches. These may be preceded by a temporary blind spot in the center of the eld of vision, usually lasting about ten minutes, and sometimes followed by facial pain under the eyes. After the blind spot vanishes, there may be zigzag streaks through the vision that may last up to hours. Even in the same person, there may be extreme variations in the headaches themselves. They may be quite severe with nausea or they may be virtually nonexistent. Migraines of most individuals have causes other than B12 deciency, but migraines of certain individuals diminish or stop completely after they are treated for B12 deciency. 12. Irritability and/or depression and/or personality changes. 13. subacute combined degeneration of spinal cord.

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24. . there was a diagram of the brachial plexus so make sure you review that. I don't quite remember what the question was but I think you have to identify the musculocutaneous nerve and label it on the picture. Rob Thomas Drinks Cold Beer- Root Trunk Division Cords Branches 5 Roots form 3 Trunks: C5 + C6 Superior trunk C7 Middle trunk C8 + T1 Inferior trunk Trunks then divide into anterior and posterior cords: All the posterior cords unite into the posterior cord Anterior cord of Superior and Middle trunk unite into the lateral cord Anterior cord of inferior trunk gives Medial cord Cords give branches: Lateral Cord Gives Musculocutaneous and a middle branch that unites with middle branch from medial cord to form the MEDIAN nerve Medial Cord Gives Ulnar nerve and a middle branch that unites with middle branch from lateral cord to form the MEDIAN nerve Posterior cord Gives Axillary nerve and Radial Nerve 25.) A 55-year-old man with hypertension, weakness in his left, lower face, and left upper and lower extremities. He has a positive Babinski sign on the left side. The question asks which is the site of the lacunar infarct. They show an image of an MRI scan of a normal brain with letters labeled over the corpus callosum, caudate nucleus, thalamus, and posterior internal capsule. Sophies CVA Handout: Pure motor weakness, without any cognitive, sensory, or cranial nerve dysfunction, occurs most often from occlusion of a small vessel (perforating branch) in the internal capsule or basal portion of pons. This is commonly found in the setting of hypertension, atherosclerosis, and diabetes and they are called lacunar strokes. LACUNAR INFARCTS (small-vessel infarcts) They are small infarcts that result from occlusion of the small penetrating branches of the larger arteries, causing small cavities (called lacunes). Because of their small size and their frequent location in relatively silent areas of the brain, many lacunar infarctions are not recognized clinically. Lacunar infarcts are commonly found in persons with long-standing hypertension and atherosclerosis. Lacunar infarcts have become more rare after the introduction of effective antihypertensive therapy. Lacunar infarcts are most common in: " 1. putamen (37%) " 2. pons (16%) " 3. thalamus (14%) " 4. caudate nucleus (10%) " 5. posterior limb of internal capsule (10%)

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26.) A 7-year-old girl has ataxic movements of the right extremities, nystagmus and diminished movement of her right vocal cord. Where is the lesion? A. Dorsal column nuclei B. dorsolateral medulla C. dorsolateral midbrain D. internal capsule E. primary motor cortex This sounds like Wallengberg syndrome BRS. P. 445 Wallenberg syndrome Condition characterized by hoarseness, cerebellar ataxia, anesthesia of ipsilateral face and contralateral body and cranial nerve signs of dysarthria, dysphagia, Dysphonia, vertigo, and nystagmus; results from infarction of the lateral medulla due to occlusion of the vertebral artery or its major branch, the PICA; Horners syndrome is frequently found on ipsilateral side. 27. 55 year old female depressed, red from her job, suicidal tendencies, jerky movements of arms, Deep tendon reexes however are brisk !!! a) Creutzfeldt-Jakob disease !!! B) Alzheimers disease !!! C) Schizophrenia D)Huntington Chorea e)Parkinsons disease Huntington Chorea refers to involuntary movements that are purposeless, quick jerks that may be superimposed on voluntary movements. Huntingtons chorea exhibits autosomal dominant inheritance (chromosome4) and is characterized by degeneration of indirect pathway GABA neurons and AEh neurons in the striatum, in particular the head of the caudate nucleus., Huntingtons disease may affect the cognitive and limbic basal ganglia pathways. Patients with Huntingtons disease may exhibit changes in mood or character in the form of irritability or impulsive behavior because of a loss of GABA neurons in the cognitive pathway. K. Thompson Hand out p. 35 Huntingtons Disease Hyperkinesia (spontaneous involuntary movements) gross wasting of caudate/putamen, also some loss of cortical neurons chorea: rapid, jerky, movements that are fragments of purposeful movt. athetosis: a type of chorea denoted by uncontrolled writhing and sinuous movements dystonia: abnormal postures caused by a joint forced into a locked position for a long period of time dementia (subcortical dementia) depression (suicide) Gene identied (chromosome 4, autosomal dominant). Produces the cytoplasmic protein Huntingtin, which induces apoptosis (programmed cell death) in striatal neurons. Fatal after 10-15 years; no treatment currently.
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28. NMDA glutamate receptor contributes to potentiation and toxicity. This is because: A) it excites with Mg2 b) gets inactivated with glycine c) is more sensitive to glutamate than aspartate d) membrane is more sensitive when hyperpolarized e) when membrane is excited, it is more permeable to Ca2+ RM. P.39 Glutamate-induced excitotoxicity: (normally occurs in ischemic neurons in stroke patients) Excesive levels of glutamate result from an increase in the inux of Ca2+ into the postsynaptic cell at NMDA receptors. The inux of Ca2+ may result in the production of free radicals in the postsynaptic cell, which damage the membranes of its organelles and the plasma membrane. Disruption of the plasma membrane results in an inux of water, which leads to swelling and eventual lysis of the cell. 29. They are testing someone's neurological response by putting them in a chair and spinning them to the right... you have to then choose from a diagram which a pattern for what the eyes would be doing. !--the answer was that the eyes would be initially turning to the left. (the concept is FOSS.... rst opposite then same) Rotation tests: http://www.vestibular.org/vestibular-disorders/diagnostic-tests/rotation-tests.php Besides ENG (electronystagmography), rotation tests are another way of evaluating how well the eyes and inner ear work together. The inner ear sends signals about head movement to the brain, causing signals to be sent to the muscles of the eyes via the vestibulo-ocular reex (VOR). For every head movement in one direction, there is eye movement in the opposite direction. With rotation tests (which employ the same type of sticky-patch electrodes or goggles used for ENG), the examiner can record eye movements while the head is moving at various speeds. This provides additional information, beyond the ENG, about how well the balance organs are functioning, along with their connections to the eye muscles. Not all people in the diagnosis phase will need rotation tests. There are two kinds of computerized rotation tests: auto head rotation and rotary chair. In auto head rotation tests, the person being tested is asked to look at a xed target and move his/her head back and forth or up and down for short periods of time. During rotary-chair tests, the computerized chair moves for the person being tested. For safety, a harness is worn and the head is restrained against a headrest. Rotary-chair testing usually takes place in a darkened room. A microphone and speaker in the testing room allow voice contact with the examiner, who is seated at a computer console just outside the door. As in ENG testing, while the eye movements are recorded, the person being tested will be asked a series of simple questions that are meant to keep the mind busy and alert during the tests. Not all rotation testing is computerized. In some cases a swivel chair is used, or the doctor or other examiner simply moves the person's head with his or her hands while observing the eye movements.

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30. It was a picture of a neutrophil and had arrows pointing to different organelles. It asked which letter represented the location where chemical signals are transformed into electrical stimuli. Myself and many others put C. No entiendo la pregunta

FALTAN 31 y 32 33. Loss of smell (anosmia).where is the problem? " Frontal lobe 34. Loss of vision in temporal visual region.where is the neoplasm? Pituitary See the question above asking about bitemporal hemianopsia 35. Patient with impaired memory loss has decreased Ach due to loss of neurons in which region?
this is a question but i didnt know the answer, look it up

Forebrain basal neurons (?) Basal Forebrain constellation (in telencephalon); medial septal nuclei and Basal nucleus of Meyenart, Dorsolateral Tegmentum of Pons (These structures are all where ACH is localized- Siegel and Sapru)

36.13y/o boy doesnt take insulin for DM, what is the second source of energy for brain after glucose? " $ When glucose availiability is low, brain uses ketone bodies to aid in fullling needs. ***option en el exam era-! beta-hydroxybutyrate***
that is the answer!

37. Sleep- old lady complains of not resting well. Using the graphs (shown below) of normal sleep patterns, explain why.
answer

Because the elderly tend to have more awake moments during the night. Explanation and graphic from previous brainstorm: Pineal Gland y/o un Pinealoma suelen causar sleep disorders. REM is affected by low Serotonin level which produces less melatonin. This is caused by light and may lead to insomnia and depression. En viejitos buscar la graca con mayor wake periods y menor stages 3 y 4. (la graca de abajo) 38. A child steps on a nail and leg reex pulls the leg away. What is the reex that contracts the other leg and prepares it to balance the rest of the body? (BRS physiology 3rd edition p. 57) Flexor Withdrawal Reex
answer

If you have ever touched a hot object or stepped on a sharp object and withdrawn your hand or foot, you have experienced a exion reex, a nocifensive reex, or a withdrawal reex, all terms describing the same event. The protective result of this
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reex is obvious; it quickly removes the part of the body from the vicinity of the offending object by contracting the appropriate muscles, usually exors, and relaxing extensor muscles (again, reciprocal innervation). The vigor of the reex depends upon the strength of the stimulus. A weak pinch produces exion of the foot; a slightly stronger one, exion of both the foot and the leg; and a very strong one, exion of foot, leg, and even hip. This spread of the reex with stronger stimulation is called irradiation. The exact nature of the limb movement and the nal position of the limb vary depending upon the site of stimulation. This phenomenon is often called local sign. Because of local sign, the withdrawal of the limb from damaging stimuli is usually appropriate in both magnitude and direction. 39. Bebe de 2 dias de nacido tiene seizures. Se le hace un MRI y se encuentra ventrculos laterales agrandados y los ventrculos dorsales separados por el agrandamiento del tercer ventrculo. ANSWER: Stenosis of the Cerebral Acueduct
question said something about third ventricle being big or something

Congenital hydrocephalus applies to the ventriculomegaly that develops in the fetal and infancy periods, often associated with macrocephaly. The most common causes of congenital hydrocephalus are obstruction of the cerebral aqueduct ow, Arnold-Chiari malformation or DandyWalker malformation. These patients may stabilize in later years due to compensatory mechanisms but may decompensate, especially following minor head injuries. During these decompensations, determining the extent to which any new neurological decits may be due to the new acute event, compared with hydrocephalus that may have gone unnoticed for many years, is difcult. http://emedicine.medscape.com/article/1135286-overview

40. Mujer guiando por la autopista le da este sendo miedo y se pone bien emocional. Tuvo un accidente de auto por ese lugar hace un ao, que parte del cerebro regula el miedo???? ANSWER: Amygdaloid (cuando cojan el examen van a entender porque no me acuerdo de la respuesta) Estaba en BS viejos, chequeenlo!
i forgot the question but i know the answer was Amygdaloid

The distinction between conscious and unconscious memory suggests - and it is generally accepted - that emotional memory involves two brain systems. While conscious memory is mediated by the hippocampus, the amygdala is implicated in emotional memory. A small collection of nuclei in the center of each temporal lobe, the amygdala controls the fear response, receiving and integrating sensory input to determine the level of threat. If the input is sufciently intense to initiate an action potential, the amygdala triggers other areas of the brain that induce the physiological response that humans interpret as fear; the danger has been "recognized." The amygdala, though, is involved not just in the fear response, but in the memory of fear, as well. In one test, researchers used functional MRI scans to measure amygdala activity while showing subjects a number of frightening and neutral images. They found that the degree of amygdala activity was a good predictor of both fear level (as reported by the subject) and of the ability several weeks later to recall having seen the image. This evidence, along with other studies with similar ndings, has made the amygdala the target of much anxiety-disorder research but it continues to raise the question of mechanism. The answer, partial though it may be, appears to lie in classic fearconditioning and in the neuronal property called long-term potentiation (LTP).

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http://serendip.brynmawr.edu/bb/neuro/neuro01/web1/Burdick.html 41)Daban una vieta de una mujer con los sintomas de myasthenia gravis. Neostigmine es un medicamento que se utiliza para: Myasthenia Gravis Myasthenia Gravis
i dont recall this being a question , but it might have been so i guess thinkneostigmine= myasthenia gravis

What is myasthenia gravis? Myasthenia gravis (MG) is a complex autoimmune disorder in which antibodies destroy neuromuscular connections. This causes problems with the nerves that communicate with muscles. MG affects the voluntary muscles of the body, especially the eyes, mouth, throat and limbs. The following are the most common symptoms of myasthenia gravis. However, each individual may experience symptoms differently. Symptoms may include: visual problems, including drooping eyelids (ptosis) and double vision (diplopia), about two thirds of people with MG have symptoms like these at rst severe muscle weakness and fatigue that may vary rapidly in intensity over days or even hours commitment of facial muscles resulting in a mask-like, a smile may appear more like a grunt difculty in swallowing and / or in pronunciation of words and neck weakness, or limb Clinical Tests There are two special clinical tests that the doctor might perform looking for MG. These are the ice test and the Tensilon test. In the ice test the doctor will examine for improvement in eyelid drooping after covering the eye for a minute or two with an ice pack or a cold pack. In the Tensilon test the doctor will examine for improvement in any weak area of the body after administration of the medication Tensilon. This medication only works when injected into the vein, and only has a short duration of effect. Variations on this test include the injection of neostigmine, and taking a tablet of Mestinon, again see if there is any improvement of weakness. Obviously both the ice test and the Tensilon test require something abnormal to be present at the time of the test, in other words the tests cannot be done if there are no abnormal ndings on examination at the time. http://www.myasthenia.org.au/html/diagnosis.htm

42) De que se compone el mecanismo de transporte de viruses para lelgar al cell body (retrograde transport) respuesta: Dyenin (the previous answer was wrong) Fast retrograde axonal transport is also involved in some pathological conditions. For example, the herpes simplex, polio, and rabies viruses and tetanus toxin are taken up by the axon terminals in peripheral nerves and carried to their cell bodies in the central nervous system (CNS) by rapid retrograde transport. Siegel and Sapru Some microtubule-directed movements, such as retrograde axonal transport or the transit of endocytotic vesicles of the plasma membrane to lysosomes, are in the direction opposite to most kinesin-dependent movements. A second group of motor proteins, the dyneins, were found to be responsible for movement toward the (#) end of microtubules. Dyneins are exceptionally large, multimeric proteins, with molecular weights exceeding 1,000,000. They are composed of two or three heavy chains (MW 470,000!!540,000) complexed with a poorly determined number of intermediate and
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remmeber something like this, but dont really remember wut it was asking

light chains. As summarized in Table 19-2, the dyneins are divided into two functional classes: cytosolic dynein, which is involved in the movement of vesicles and chromosomes, and axonemal dynein, which is responsible for the beating of cilia and agella (discussed later). http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=mcb&part=A5452 43. Bacterial Meningitis, given symptoms of a patient (e.g. cloudy CSF, protein count) and asked to name the type of condition. The answer was bacterial meningitis. Q: What are the signs and symptoms of meningitis? A: High fever, headache, and stiff neck are common symptoms of meningitis in anyone over the age of 2 years. These symptoms can develop over several hours, or they may take 1 to 2 days. Other symptoms may include nausea, vomiting, discomfort looking into bright lights, confusion, and sleepiness. In newborns and small infants, the classic symptoms of fever, headache, and neck stiffness may be absent or difcult to detect. Infants with meningitis may appear slow or inactive, have vomiting, be irritable, or be feeding poorly. As the disease progresses, patients of any age may have seizures. http://www.cdc.gov/meningitis/about/faq.htmlxss+ssssz+xxz CSF analysis should be carried out in all patients with suspected meningitis as long as there is no contraindication to the procedure. Normal values include an opening pressure of 90 to 180 mm H2O; 0 to 5 lymphocytes/L; glucose and protein concentrations of 50 to 75 mg/dL and 15 to 40 mg/dL, respectively; and simultaneous CSF:blood glucose ratio greater than 0.6. Typical CSF ndings in patients with bacterial meningitis include an opening pressure of greater than 180 mm H2O; 1000 to 5000 leukocytes/L (80% or more of which are neutrophils), glucose and protein concentrations of 40 mg/dL or less and 100 to 500 mg/dL, respectively; and simultaneous CSF:blood glucose ratio of 0.3 or less. However, there is considerable overlap of the CSF ndings in bacterial, nonpyogenic, and noninfectious meningitis. CSF measures that are highly predictive of a bacterial cause include a WBC count greater than 2000/L; a neutrophil count greater than 1180/L; a CSF:blood glucose ratio of less than 0.23; and glucose and protein concentrations of less than 34 mg/dL and less than 220 mg/dL, respectively. http://www.medscape.com/viewarticle/451596_2 45- 35 yr old man had unilateral C-2 spinal cord transection. He is most likely to have 1. Erectile disfunction i put the one that had something to do with upper 2. Bradicardia part of body sinces it C2 3. Constipation (the answer choice thats "dont remember" lol 4. Lack of sweat 5. Dont' remember Mano esta no estoy seguro. Pero bueno, busque informacin por internet sobre C2 hemisection y lo nico que encontr fue que las personas con este tipo de lesin tenan problemas respirando por que tenan da~o a los nervios Quizas la que dice dont remember era la contestacin Si alguien encuentra algo mejor favor demandarlo. ABSTRACT: Upper cervical spinal cord injury (C2 hemisection) results in paralysis of the ipsilateral hemidiaphragm due to the interruption of descending respiratory premotor neurons. After C2 hemisection, however, it is not clear what happens to inspiratory intercostal muscle activity. Innervation of the diaphragm primarily involves
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exact question

monosynaptic bulbospinal premotor neurons, whereas innervation of thoracic intercostal muscles involves primarily respiratory thoracic interneurons. Studies show that at least 60% of the respiratory interneurons project to the contralateral ventral horn. Therefore, we hypothesized that intercostal activity may persist ipsilateral to a C2 spinal cord hemisection. 46- A drug changes the cell membrane potential from -60mV to -45mV. The drug most likely: 1. Activates channels Na 2. Activates channels K exact 3. Activates channels Cl question 4. Close channels Na 5. Close channels K 6. Close channels Cl - A brief stimulation of the resting membrane will cause the membrane to briey depolarize (for example from 70 to 60), but itwill return to the resting potential. More stimulation (lets say to 50) will reach threshold and start an action potential (AP). The threshold phenomenon makes action potentials all-or-none. Either you have an AP or you do not. (Think of a toilet. Not only does it have threshold, but also refractoriness.) What is happening at threshold? Threshold is the point at which the Na current is equal to the K current. A small depolarization will cause some Na channels to open, but not enough to overcome the resting K current. If a depolarization induces more Na current than K current, the sodium cycle will develop: Na channels open sodium enters depolarization This cycle causes the rapid depolarization of the upstroke of the AP, entirely due to Na. The membrane comes close to the Na equilibrium potential, but the Na channels inactivate after a short period of time, and the Na current stops. 47. 30 yrs AIDS patient with malignant CNS lesions. They performed a stereotactic biopsy. No other malignancy is found in the body. What would be the most likely CNS malignancy?
dont rememebr for sure if this is a question, but dont know the answer

Este slide lo consegui de un lecture de Harvard medical school. Basicamente el lecture era de las condicionesneurolgicas que se podan desarollar a consecuencia de Aids. Aqu el profesor highlights the most important 3 conditions that could be as a result of Aids.

48. 40 yr old presented with burning sensation in feet. He also had decreased pain and temp sensation in his feet. And decreased ankle reex. What lab test would you run to make a diagnosis?
didnt know the answer but this is a question

They didnt give me much to work with here cause of the lack of answer choices. However, Decreased pain and temperature sensation suggests a lesion in the anterolateral system sensory system which carries pain and temperature sensation. The decreased ankle reex suggests a lower motor neuron lesion (remember hyporeexia is lower motor neuron, hyper: UMN).

51. A substance is injected in the brain of an animal model which causes seizures. Which substance is it? this was a question, gure out the answer a. Adenosine
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b. GABA c. Something, I cant remember d. Glutamate e. Dopamine Esta ya estaba contestada, and I agree with the answer considering glutamate is the main excitatory neurotransmitter in the brain. Glutamic acid has been implicated in epileptic seizures. Microinjection of glutamic acid into neurons produces spontaneous depolarisations around one second apart, and this ring pattern is similar to what is known as paroxysmal depolarizing shift in epileptic attacks. This change in the resting membrane potential at seizure foci could cause spontaneous opening of voltageactivated calcium channels, leading to glutamic acid release and further depolarization. 52. A patient 27 years old with Downs Syndrome. What is the condition she is more prone to in the next decade. answer: dementia Down syndrome increases the risk of Alzheimers disease. People with Down syndrome may experience health problems as they age that are similar to those experienced by older people in the general population. The presence of extra genetic material found among persons with Down syndrome may lead to abnormalities in the immune system and a higher susceptibility to certain illnesses, such as Alzheimer's, leukemia, seizures, cataracts, breathing problems, and heart conditions. These factors can contribute to a shorter life expectancy for people with Down syndrome. One study, carried out in the United States in 2002, showed an average lifespan of 49 years, with considerable variations between different ethnic and socio-economic groups. However, in recent decades, the life expectancy among persons with Down syndrome has increased signicantly up from 25 years in 1980. The causes of death have also changed, with chronic neurodegenerative diseases becoming more common as the population ages. Most people with Down Syndrome who survive into their 40s and 50s begin to suffer from an Alzheimer's disease-like dementia. 55. Cual es el stimuli del cross-extensor reex and withdrawal reex Ans. painful stimuli to nocireceptor of the skin. Veried.!

question- cross extensor and withdrawal reex answer- painful stimuli to nocireceptor of skin

56:!The!glial cells!serve to support the neurons. !Some estimate that glial guided migration accounts for 90% of neuronal migration in humans. !This could be the relevant answer in terms to!mental retardation. !Likely cause of mental retardation: yeah question was about mental retard, and what !!!! It's is about glial cells out answer !!!! Ans: it could be!neural migration!or neural proliferation 57: Taste and the tongue: which nerve innervates posterior 1/3? Anterior 2/3: CN7 Posterior 1/3: CN9 Epiglottis: CN11 58: !Subthalamic nuclei and Globus Pallidus: there is no real question here. !Here is the strongest link I could nd between the two. !Perhaps the question deals with Parkinsons?
question asked- what is linked to parkinsons or some shit, and in the answer both subthalamic nuclei and globus pallidus was there, so WHICH IS IT FOR SURE? look it up

happens in that case, i didnt know this shit, gure

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Lateropallido-subthalamic system Strong reciprocal connections link the!subthalamic nucleus!and the external segment of the globus pallidus. Both are fast-spiking pacemakers. Together, they are thought to constitute the "central pacemaker of the basal ganglia"[13]!with synchronous bursts. The connection of the lateral pallidum with the subthalamic nucleus is also the one in the basal ganglia system where the reduction between emitter/receiving elements is likely the strongest. !The lateropallido-subthalamic system is thought to play a key role in the generation of the patterns of activity seen in!Parkinson's disease. 59: not listed 60: not listed 61. Paciente con confusin y retencin urinaria, un examen demostr que tenia bilateral midriasis, dry skin, and dry mouth. Que ocurra? question listed that the pt had confusion, Answer: !- adrenergic activation * Confusion ,Urinary Retention, Midriasis, Dry Skin, Dry Mouth Sympathetic Innervation !- adrenergic activation !1 receptor Specic actions of the $1 receptor mainly involves smooth muscle contraction. It causes vasoconstriction in many blood vessels including those of the skin, gastrointestinal system, kidney (renal artery)[6] and brain[7]. Other areas of smooth muscle contraction are: ureter vas deferens hair (erector pili muscles) uterus (when pregnant) urethral sphincter bronchioles (although minor to the relaxing effect of %2 receptor on bronchioles) blood vessels of ciliary body (stimulation causes mydriasis) Further effects include glycogenolysis and gluconeogenesis from adipose tissue[8] and liver, as well as secretion from sweat glands[8] and Na+ reabsorption from kidney.[8] negative feedback in the neuronal synapses " Wikipedia * Dry mouth and dry skin? Dry mouth because parasympathetic innervates salivary glands, so therefore sympathetic activation would decrease salivation. * Confusion The antidepressants doxepin and imipramine have anticholinergic effects, as well as alpha- and beta- adrenergic stimulant effects. Benet from these agents may take several weeks. Current research indicates that calcium channel blockers and beta agonists (such as terbutaline) may be useful, as well. However, anticholinergic effects of many of these medications may limit their use in the elderly. In addition, these agents should be used cautiously in patients with dementia, as they can increase confusion.2 " American Society of Consultant Pharmacists
urinary retention etc.

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62. Paciente con spasticity, un MRI se le encontr una edema con shift del cerebro hacia la derecha. What are the histological ndings in the patient? * The particular vulnerability of white matter to vasogenic edema is not well understood; probably its loose structural organization offers less resistance to uid under pressure than the gray matter. Possibly also, it is related to the special morphologic characteristics of white matter capillaries. The accumulation of plasma ltrate, with its high protein content, in the extracellular spaces and between the layers of myelin sheaths would be expected to alter the ionic balance of nerve bers, impairing their function. By contrast, in cytotoxic edema, all the cellular elements (neurons, glia, and endothelial cells) imbibe uid and swell, with a corresponding reduction in the extracellular uid space. This type of edema occurs typically with hypoxic-ischemic injury. The effect of oxygen deprivation is to cause a failure of the ATP-dependent sodium pump within cells; sodium accumulates in the cells, and water follows (Fig. 31-1B). The term cellular edema is preferable to cytotoxic edema because it emphasizes the cellular swelling rather than a toxic factor in the genesis of the brain edema. When it occurs in pure form, it is most often due to hypoxia, but it may also complicate acute hypo-osmolality of the plasma, as occurs with dilutional hyponatremia, acute hepatic encephalopathy, inappropriate secretion of antidiuretic hormone, or the osmotic disequilibrium syndrome that occurs with hemodialysis(page 1189). $ Adams and Victor Principles of Neurology 7th ed. Ch. 38 Page 523

dont understand this spanish question but might have been a question on it.

* Histological changes of brain oedema were observed as early as 6 h postburn, accompanied by swelling of endothelial cells and perivascular astrocytes. Vacuolation look place in neurons 12 h post-burn, with ischaemic necrosis of varying degree of the capillary endothelium, neurons, and axons. 'these changes became more marked with the lapse of time. The BGS group showed the most obvious consequences mentioned above 24 h post-burn. The results indicated that the model of brain oedema after severe burn had features of both vasogenic oedema and cellular toxic oedema as regards MRI and pathology. " http://www.medbc.com/annals/review/vol_14/num_1/text/ vol14n1p44.htm 65. A 26 year old woman with a previous case of an anencephalic birth arrives for the rst time at the physician at 20 weeks gestation. Which component of blood serum is best to diagnose!the likelihood of a!repeated fetus abnormality. ! a.!estriol b. alpha-feto protein (answer) c. folate d. Human Chorionic Gonadotrophin (HCG) e. TSH * Anencephaly This is one of the most frequent and also most appalling congenital malformations of the brain. Its incidence is 0.1 to 0.7 per 1000 births, and females predominate in ratios of 3:1 to 7:1. The concordance rate is low, being the same in identical and fraternal twins, but the incidence of the malformation is several times the
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expected rate if one child in the sibship has already been aficted. Anencephaly is more frequent in certain geographic areas, e.g., Ireland. Lacking are large portions of scalp, cranial bones, and brain, both cerebral cortex and white matter. All that is seen is a hemorrhagic nubbin of nerve, glial, and connective tissue. Brainstem, cerebellum, and spinal cord are present, but often they too are malformed, as are the heart and other organs (15 to 40 percent of cases). In anencephalics who survive for a few days (65 percent die in utero and almost 100 percent before the end of the rst postnatal week), startle reactions may be observed, as well as movements of limbs, spontaneous respirations, pupillary light reactions, ocular movements, and corneal reexes. In a few, avoidance reactions, crying, and feeding reexes can be elicited. This condition can be anticipated if the mother's serum levels of afetoprotein and acetylcholine esterase are elevatedeven more reliably if testing is done on amniotic uid. Positive tests should lead to ultrasound imaging of the fetus. Hydramnios is common. Apparently, the causes of anencephaly are multiple and include chromosomal abnormalities, maternal hyperthermia, and deciencies of folate, zinc, and copper (see Medical Task Force on Anencephaly in the References). There is fairly secure evidence that supplemental intake of folic acid during the rst trimester of pregnancy (i.e., from the time of conception) greatly reduces the incidence of anencephaly and myelomeningocele. $ Adams and Victor Principles of Neurology 7th ed. Ch. 38 Page 523 66. 2 yr old . . . distended abdomen . .. constipation . . . distended colon . .. What causes defects ? Answer: failure of migration of neural crest cells (Hirschprung Disease) * The human syndrome congenital megacolon (Hirschsprung disease) closely resembles an animal model in which excess extracellular matrix molecules are present in the colon. This results in aberrant migration of neural crest derived cells. In this animal model, and in Hirschsprung disease, neurons forming the enteric ganglia fail to migrate into the lower bowel. In absence of these cells, no sensory signal indicating the absence of these cells, no sensory signal indicating the presence of feces in the colon is sent to the CNS. Therefore, no motor signal is sent to control defecation. " Haines. Fundamental Neuroscience 2nd ed. Ch 5 P 80-81 67. Horner SYMPTOMS: Horners Syndrome miosis, hemianhydrosis, mild ptosis, enophthalmus (retraction of $ eyeball into head) NOTA: Horners syndrome es perdida de estimulacion sympatica al ojo por $ lo tanto el oculomotor CN III esta trabajando solo A lesion of the descending hypothalamic axons between the hypothalamus and the preganglionic sympathetic neurons in the T1 spinal segment may result in Horners syndrome. Horners syndrome is caused by disruption of a hypothalamic/sympathetic pathway, which provides sympathetic innervation to the sweat glands in the face and scalp, blood vessels in the head, and the superior tarsal and dilator pupillae muscles in the orbit. Patients with Horners syndrome have miosis (pupillary constric- tion), ptosis (drooping
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know the tract- i think the answer was descending hypothalamic tract

eyelid), and anhidrosis (lack of sweating), signs that are always ipsilateral to the side of the lesion. Patients may also have orthostatic hypotension in which there is a signicant drop in systemic blood pressure when the patient changes from a lying to a standing position. A lesion of the bladder control axons from the pons above sacral levels S2 through S4 may result in a spastic bladder. In these patients, sacral parasympathetic neurons that innervate the bladder are not inhibited effectively when the bladder is stretched during lling. The bladder contracts in response to a minimum amount of stretch, causing frequent involuntary reex emptying. RM. P. 76-77 68. Use of pilicarpin Pilocarpine has been used in the treatment of chronic open-angle glaucoma and acute angle-closure glaucoma for over 100 years.It acts on a subtype of muscarinic receptor (M3) found on the iris sphincter muscle, causing the muscle to contract and engage in miosis. Pilocarpine also acts on the ciliary muscle and causes it to contract. When the ciliary muscle contracts, it opens the trabecular meshwork through increased tension on the scleral spur. This action facilitates the rate that aqueous humor leaves the eye to decrease intraocular pressure. Pilocarpine is often used as an antidote for scopolamine, atropine, and hyoscyamine poisoning.Pilocarpine is also used to treat dry mouth (xerostomia. Pilocarpine stimulates the secretion of large amounts of saliva and sweat. Pilocarpine is used to stimulate sweat glands in a sweat test to measure the concentration of chloride and sodium that is excreted in sweat. It is used to diagnose cystic brosis (CF). En resumen: Pilicarpin es un tratamiento para glaucoma, que actua en receptores mucarinicos (m3) de los msculos del sphinter de la iris y msculos ciliares, ayudando a la contraccin (miosis). Acelera la razn a la que el humor acuoso sale del ojo, de esta manera disminuyendo la presin intraocular. (WIKI, sry por la referencia) 75. A man moving snow slips and receives trauma to the left side of the brain He presents with Left sided Hemiplegia, which resulted in hemorrhage. CT at the left ventricle. Answer: i put something with epilespsy
i know this was a question but i didnt know answer

so i guess the answer is that it STIMULATES SWEAT GLANDS

As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reexes and decreased endurance. (wikipedia) Possible causes of contralateral hemiplegia: A lacunar stroke involving the posterior limb of the internal capsule may result in a complete contralat- eral anesthesia, contralateral hemiplegia, contralateral homonymous hemianopsia, and a slight bilateral hearing loss. A lacunar stroke involving the genu of the internal capsule may result in contralateral lower face weakness, transient deviation of the uvula toward the lesion, and deviation of the tongue away from the lesion on protrusion. RM. P. 214-215

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76. Lesion of the stellate ganglion, caused by a Pancoast Tumor (towards the apex of the lung)....(describing symptoms of a horner's patient) ALSO important to be able to recognize the other symptoms of Horner's.. bc there are several of them throughout. What symptoms are expected to be seen in this patient? Answer: ptosis, anhydrosis, and the other symptoms of horner's
? has some bs about pancoast tumor, and pick the option with symptoms of horners

Aside from cancer general symptoms such as malaise, fever, weight loss and fatigue, pancoast tumor can include a complete Horner's syndrome in severe cases: miosis (constriction of the pupils), anhidrosis (lack of sweating), ptosis (drooping of the eyelid) and enophthalmos (sunken eyeball). In progressive cases, the brachial plexus is also affected, causing pain and weakness in the muscles of the arm and hand. The tumor can also compress the right recurrent laryngeal nerve, and from this a hoarse voice and bovine cough may occur. (wiki)

77) A 50 year old painter wakes up from a nap after 2 hours with numbness in his arm. !He has weak extensors of the arm, wrist, a weak brachioradialis. !What is affected? Radial nerve is the answer??? A. Radial N B. Brachial plexus C. C 8 D. Cervical cord E. Cerebral hemisphere ! Despite the bulk of the muscle body being visible from the anterior aspect of the forearm, the brachioradialis is a posterior compartment muscle and consequently is innervated by the radial nerve. (wikipedia) 78 tenias que saber q pasa con el CSF en hemorragia Red blood cells may be present in CSF as a result of a subarachnoid hemorrhageor a bloody lumbar they gave lab values- puncture. RM.P. 25
i didnt know this shit, but i assumed RBC would be increased , and in question it said glucose was normal, and i dunno bout lymphocyte value

CSF during hemorrhage: I imagine this must be a sub-arachnoid hemorrhage or it wouldn't really affect the make-up of the CSF. As you can see below, the main difference is the presence of RBC's. Three samples must be taken to determine the RBC's are present in equal amounts and not decreasing (which means they are coming from a nicked artery during puncture procedure. Normal: Clear, <5 lymphocytes/mm3, protein <45 mg/dl, glucose >45 Sub Hemm: Bloody color, RBC's present (5x10^6/mm), protein normal to slight elev, Glucose= normal.

79. A 69-year-old man is being treated in the hospital for major depression, presents mental lability and periods of laugh and cry. He has a 2 year history of progressive disorder and short- term memory loss. Developed left hemiparesis and bilateral extensor plantar reex. What is the diagnosis?
dont know the correct !!!!!! A) Multi- infarct dementia yo puse esta answer for this

!!!!!! B) Subdural hematoma

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!!!!!! C)Pseudodementia due to depression - !Pseudodementia is a syndrome seen in older people in which they exhibit symptoms consistent with dementia but the cause is a pre-existing psychiatric illness rather than a degenerative one. ***He was already being seen for depression and I think that points more towards this answer. also, his mental lability would indicate pseudodementia over true dementia. This seems important for us to know because pesudodementia due to depression is a treatable condition while dementia is not. 80: Toxin that evokes the Acetylcholine release by exocytosis, presents a decrease in: A) Amount of smooth muscle in the motor end plates. (No, would not affect # of muscles) B) Number of mitochondria in the motor end plates. (No) didnt know the C) Number of acetylcholine receptors in post synaptic neuron. (I am not sure if this answer to this one, number can change so rapidly but if anything it would increase) but maybe D D) Number of synaptic vesicles in motor end plates. (This clearly decreases as vesicles are released and ACh released) E) Number of microtubules in post synaptic neuron. (No) 81. patient!injects himself with tetanus-botulism agent what does it interfere with? Union of synaptic vesicles to presynaptic membrane (ie tetanus toxin binds to synaptobrevin which prevents exocytosis of neuotransmitter) 82. Increase intraocular pressure?!
? talks about pt w/ glaucoma and what happens? increase intraocular pressure

Blockage of canal of Schlemm, leads to glaucoma 83. Diagrama con area de substantia nigra marcada con X. What does the lesin/ damage in this marked area represent? " Alzheimer/dementia " Wilson " Huntington " Parkinson- degeneration of neurons of substantia nigra, pars compacta; depletion of domapine in caudate nucleus and putamen. 84. R pupil dilation with NO accommodation reex. L plantar extension reex. Where is the lesion? " R dorsolateral medulla" L dorsolateral medulla didnt know " R ventrolateral medulla this one " L ventrolateral medulla " R dorsolateral pons " L dorsolateral pons " *** es una de esas cuatro pq la lesion es en medulla pero noc cual*** 85. lady 69yr llevada al Dr por sudden weight loss (20lbs) y varios perdidas motoras.deciencia en q vitamina? Vit B12 ( anemia)- subacute combined degeneration of spinal cord, or Lichtheims disease- refers to degeneration of myelin of the posterior and lateral spinal columns of spinal cord due to B12 deciency and is associated with pernicious anemia. 86. Diagrama de spinal cord con diagramas identicados con letras. Paciente con loss de pain & temp en LEFT leg donde es la lesin?
diagram of spinal cord and asking some shit, ! i didnt know

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Marcar en diagrama la parte de spinothalamic tract. Lateral spinothalamic tract mediates pain and temperatura sensation; axons of neuron 1 enter lissauers track and decussate in ventral white commisure to the VPL of thalmaus. Somatotopic representation means that it then projects to the medial portion of the sensory cortex. ** star pendiente a identicar bien R & L en el dibujo** 89. 67 year old man had small cell carcinoma of the lung presents with tingling in the feet and loss of muscle stretch reexes and vibratory sensation in the ankles. Man also has wobbly gait. The question asks where the lesion is located.! ! a. cerebellar vermis!"topographical maps of the trunk muscles" **Page 142 USMLE Road Map Also chemotherapy induced may lead to truncal ataxia bc it affects the vermis. b. cerebral peduncles! c. corona radiata! d. dorsal spinal cord roots! e. Ventral pons! ! 90. The question discusses a infant born with an incomplete formation of the membranous cranium and no cerebral hemispheres, mother has high levels of amniotic uid. The question asks to describe what caused the condition.! ! The condition is anencephaly caused by INCOMPLETE CLOSURE OF ROSTRAL NEURAL TUBE. The condition is associated with polyhydramnios (high amniotic uid) because infant can not swallow amniotic uid because there are no cerebral hemispheres. High alpha fetoprotein is also associated with OPEN neural tube defects ** Page 7 Road Map 91. Drawing with an X showing a lesion on part of the brainstem. Asks if lesion in this area produces: this ? was on there Contralateral ataxia = ? w/ a pic, but i didnt Ipsilateral ataxia (would be @ cerebellum) Contralateral loss of tactile and vibration sense/Ipsilateral = loss of tactile and vibration know it depends on X affects Dorsal column Medial lemniscus. Contralateral weakness and plantar reex/ Ipsilateral weakness and plantar reex = corticospinal tract babisnki positive also depends on decussation and X localization. 92. which is capable of wrapping multiple axons in a myelin sheath Astrocytes = structural support Microglial cells = phagocytose neuronal debris after CNS injury. Oligodendrocytes = form myelin for axons in the CNS, each of the processes can myelinate individual segments of many axons. ** Page 50 Road Map Satellite cells = are attened Schwann cells, a type of glial cell, lining the exterior surface of neurons in the peripheral nervous system. Satellite cells also surround neuron cell bodies within ganglia. They are thought to have a similar role to astrocytes in the central nervous system (CNS). They supply nutrients to the surrounding neurons and also have some structural function. Satellite cells also act as protective, cushioning cells. (Wiki) Shwann cells = supporting cells of the PNS, forms myelin for only a single intermodal segment of a single axon.

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93. There was a clinical case involving a man who was vomiting. It asked you which area of the brain was involved in the control of emesis (vomiting). The AREA POSTREMA in the wall of the 4th ventricle, a circumventricular organ of the brain (where there is no BBB), act as receptor to circulating toxins that may cause vomiting. **Page 21 Road Map 94. A 20 yr old man was shot in the back. The bullet transected his spinal cord at the level of T5. The man became paraplegic shortly after the lesion. What will happen to the muscles of his lower extremity 3 months after the injury? Areexia Bilateral Horner syndrome Fasciculations Hyperreexia Profound atrophy The pt has LMN lesion but since the question is what will happen 3 months after injury it has evolved into a spastic stage. (Directly from Sofys handout, page 5) Neurologically, upper motoneurons have a net overall inhibitory effect on DTRs. As a result, an UMNL combines paresis of skeletal muscles with DTRs that are hyperactive. An UMNL results in atrophy of weakened muscles only as a result of disuse, because these muscles can still be contracted by stimulating muscles stretch reexes. An UMNL is also accompanied by reversal of cutaneous reexes, which normally yield a exor motor response. The best known of the altered exor reexes is the Babinski reex. Two other exor reexes, the abdominal and cremasteric, are also lost in an UMNL. The constellation of UMNL signs combining paresis with hyperactive reexes, disuse atrophy of skeletal muscles, and altered cutaneous reexes is known as spastic paralysis (paresis) that is ipsilateral or contralateral and below the site of the lesion. If the UMNL is anywhere in the spinal cord, the resulting spastic paralysis is ipsilateral and below the level of the lesion. On the other hand, if the UMNL is above the decussation of the pyramids, the resulting spastic paralysis is contralateral and also below the level of the lesion. In contrast to upper motor neuron lesions, a LMNL will result in hypoactive DTRs and reduction in muscle tonus (hypotonicity) because lower motor neurons form the motor component of the reex. Therefore, a LMNL will result in a paresis combined with suppressed or absent DTRs. The constellation of a LMNL signs combining paresis with suppressed or absent reexes, fasciculation, and atrophy is known as a accid paralysis (paresis). With few exceptions, a LMNL will produce a accid paralysis ipsilateral and at the level of the lesion. SPINAL TRAUMA AND SPINAL SHOCK Immediately after the severe spinal injury there is often a period of total absence of deep tendon reexes, an atonic, paralyzed bladder and rectum, complete accid paralysis of muscles innervated by neurons below the lesion, and loss of all sensations below the level of the lesion. This areexic period is called spinal shock. The pt. may still be fully conscious. If the injury is below C-4, breathing should be normal, but if it is above that level, phrenic paralysis may lead to early death. Spinal shock may last weeks (1 - 6 weeks). As the period of shock clears, there is return of reexes and the pt. enters a spastic stage (i.e., the accid paralysis below the lesion is replaced by spasticity and other signs associated with an UMNL). The mechanism by which this period of spinal shock resolves into spasticity is
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not fully understood. Bladder and bowel function may become automatic (spastic, hypertonic), with emptying in response to moderate lling. 95) !Old lady has cerebral infarction (CI). !Day later complains of loss of audition in right ear. !Which of the following structures on the left side is most likely affected?
i think this was a " question but i dunno "i the answer , but " remember all these " answer choices

a. middle temporal gyrus(1ry auditory cortex) b.inferior temporal gyrus (prosopagnosia) c.medial geniculate nucleus (auditory nuclei of thalamus) d.lateral geniculate nucleus (vision) e.vestibulocochlear nerve (it would be ipsi and theyre asking for contralateral site)

96) !Old man dies after he hits a hole in one at the golf course. !Autopsy reveals neurobrillary tangles associated with dementia type alzheimers. !The degeneration of cholinergic axons that project to the cerebral cortex are found within what structure? " " " " " a.basal nucleus of meynert b.dentate nucleus c.nucleus raphe magnus d.solitary nucleus e.hippocampus

A subcortical structure of the telencephalon, the septum provides a major cholinergic input to the hippocampus. The adjacent structures nucleus basalis of Meynert, and diagonal band of Broca provide cholinergic input to the neocortex. These cholinergic projections are among the rst to degenerate in Alzheimers disease, and treatment with various types of cholinergic replacement therapy are now in vogue. **Page 87 NeuroPhys handout

97.!!!! Paciente que le remueven parotid gland? (Parotidectomy)

question had something to do with this, but i didnt know

The facial nerve divides the gland into a supercial and deep lobe. Since the facial nerve supplies all the muscles that move the face a lesion will cause paralysis. http://yoursurgery.com/ProcedureDetails.cfm?BR=4&Proc=40

98. They give you an electron micrograph and ask you to identify the neuromuscular junction. www.answers.com/topic/neuromuscular-junction-1 101. !Know the concept of diopters and what lesions can cause a person who can see -1 with BOTH eyes and +3 in ONE eye when in focus. ! The numbers may be wrong BUT the answer was macular degeneration!!! Not sure of what theyre asking

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A dioptre, or diopter, is a unit of measurement of the optical power of a lens or curved mirror, which is equal to the reciprocal of the focal length measured in metres (that is, 1/metres). Convex lenses have positive dioptric value and are generally used to correct hyperopia (farsightedness) or to allow people with presbyopia (the limited accommodation of advancing age) to read at close range. Concave lenses have negative dioptric value and generally correct myopia (nearsightedness). Typical glasses for mild myopia will have a power of #1.00 to #3.00!dioptres, while over the counter reading glasses will be rated at +1.00 to +3.00!dioptres. (from wiki) 102. !Dermatome for the perineal area. !S2-S5 http://www.svhrad.com/DigLib/Neuro/dermatomes-netter2.jpg 103. 35 yr. old woman, 1 month history of ptosis, diplopia, limited abundance/ elevation of right eye and fatigable ptosis on left. After 2 days of pyridostigmine therapy, her ocular symptoms resolve. One wk later develops fasciculations in both thighs, that are most pronounced 1 hr after she takes pyridostigmine. DESCRIPTION: Pyridostigmine Bromide Tablet is an orally active cholinesterase inhibitor Read more: http://www.drugs.com/pro/pyridostigmine.html#ixzz0nqnf3yFS Fasciculations most likely caused by excess of: A)Ach B)GABA C)Dopamine D)Epineph E)NE 104. 56 year old man, 6 month history burning sensation in feet. Sensation to pinprick, vibration + joint position ! over distal lower extrem. Ankle reexes absent. Biopsy shows ! in unmyelinated bers immunoreactive for calcitonin gene related peptide. Which is a function of these axons? Porter presentation & physio handout afferent from GT organs afferent from nociceptors X motor neuron efferent Parasympathetic efferent to BV Sympathetic efferent to sweat glands

105.! A 35 year old man is being observed while sleeping.! While sleeping the man experiences muscular atonia, variations in respiration and blood pressure, as well as a huge erection.! Is this guy experiencing: A. Narcolepsy B. Nightmares C. Normal Sleep D. Sleep Apnea E. Wet Dreams (I actually don't remember the last one)

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These symptoms are typical of REM sleep so it would be nightmares. ** Page 61 Handout In contrast to SWS, rapid eye movement sleep (REM sleep) is also called paradoxical sleep because the EEG pattern resembles wakefulness: high frequency, low voltage, desynchronized. Other aspects of REM sleep: most intense dreams inhibition of all skeletal muscles, except eyes, middle ear osscicles, and respiration. Importance: see REM behavior disorder below. penile erection in males averages 20% of sleep, but is more in young children and less in the elderly as night continues, REM periods increase in length, while stage 3-4 decrease in length. rehearsal and organization of recently experienced events (memory consolidation) 106. A 15 year old kid gets stabbed behind the knee, and four weeks later has trouble walking.!When they hook him up to a myoelectrogram, what do you expect to see? A. Electronic silence B. Giant cell motor unit potential C. Spontaneous motor unit potential D. Fibrillations (info from wiki & sofys handout) E. (Don't remember) Fibrillation also occurs with individual skeletal muscle bers.[1] This happens when muscle bers lose contact with their innervating axon producing a spontaneous action potential, "brillation potential" that results in the muscle ber's contraction. These contractions are not visible under the skin and are detectable through needle electromyography (EMG) and ultrasound.[2] Fibrillations do not occur in healthy individuals. They are a major symptom in acute and severe peripheral nerve disorders, in myopathies in which muscle bers are split or inammed, and lower motor neuron lesions. They contrast with fasciculations that are visible spontaneous contractions involving small groups of muscle bers. Also, fasciculation does not necessarily denote pathology, as does brillation, although it can be seen in lower motor neuron lesions as well. 107) Un nino nace con hidrocefalia, tiene los lateral ventricles y 3rd ventricles hinchados. Te pregunta donde esta problema. ! Answer: Cerebral aqueduct ! The mesencephalic duct, also known as the aqueductus mesencephali, aqueduct of Sylvius or the cerebral aqueduct, contains cerebrospinal uid (CSF), is within the mesencephalon (or midbrain) and connects the third ventricle in the diencephalon to the fourth ventricle, which is between the pons and cerebellum. 108) Vigneta larguisima sobre un persona que empieza con debilidad hasta no!puede mover!sus piernas y tiene areexia, paralysis de las piernas. Que tiene la persona? ! Answer: Guillain Barre Syndrome !
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Aprenderse los simtomas de un Guillan Barre. The disorder is characterized by symmetrical weakness which usually affects the lower limbs rst, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs, manifesting as "rubbery legs" or legs that tend to buckle, with or without dysesthesias (numbness or tingling). As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness, (oropharyngeal dysphagia, that is difculty with swallowing, drooling, and/or maintaining an open airway) and respiratory difculties. Most patients require hospitalization and about 30% require ventilatory assistance.[11] Facial weakness is also commonly a feature, but eye movement abnormalities are not commonly seen in ascending GBS, but are a prominent feature in the Miller-Fisher variant (see below.) Sensory loss, if present, usually takes the form of loss of proprioception (position sense) and areexia (complete loss of deep tendon reexes), an important feature of GBS. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising. These pains are self-limited and should be treated with standard analgesics. Bladder dysfunction may occur in severe cases but should be transient. If severe, spinal cord disorder should be suspected 109. 67 y/o woman cant open L eye or R arm/leg. L eye deviates outward + pupil dilated. 110. Weakness of R upper/lower extrem. Damage to which part is cause of hemiparesis . . . Shows diagram of part of brainstem labeled A-H Segun los sintomas se afecto el CNIII. El oculomotor originates at the level of the superior colliculus (midbrain). Por lo tanto la lesion debio haber sido en ese nivel. 110. Asthma study to locate preganglionic autonomic neurons that synapse upon neurons that synapse upon neurons of bronchioles. A tracer, horseradish peroxidase, is injected into bronchial wall of animal and transported retrograde to identify preganglionic neurons. Which is location of injected autonomic neurons A) DM nucleus of vagus B) Inferior salivatory nucleus C) Lateral horn thoracic spinal cord D) Superior cervical ganglion E) Superior salivatory nucleus Mi anlisis para esta pregunta es el siguiente. Estn estudiando asma que es una enfermedad causada por bronchoconsriction. Bronchoconstriction es una actividad parasympathetic. Esto se lleva a cabo a travs del vagus nerve. Dorsal nucleus of vagus mostly serves parasympathetic vagal functions in the heart, gastrointestinal tract, lungs, and other thoracic and abdominal vagal innervations.

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