Neurological symptoms

HEMIPLEGIA
RIGHT HEMIPLEGIA

• Cortical
• Test for Aphasia (think of cortical lesions;
also know province and background)
• Name objects (eg. Pen,tie,etc.); repeat (no.
if’s, and’s or but’s); read and check
comprehension; listen to spontaneous speech
for errors
• Check cortical sensory loss
• Position sense, point localization,
graphesthesia (write number on palm);
stereognosis (coin, pen comb)
• Are face and arm more involved than leg? (Middle
cerebral AA territory) or Is leg more involved? (Anterior
cerebral artery)
• Is there eye deviation?
• Eyes deviate to hemisphere involved and away from
the hemiparesis in cortical lesions
• Check field defect
• NB: field defect suggests subcortical deficit except
when occipital lobe is involved in which case the field
defect is due to a lesion in the cortex.
• “Cortical” type eye deviation maybe found in
subcortical lesions
• Hemiparesis and seizure suggest cortical lesion
• Determine if lesion is of same distribution as the
weakness
• Normal primary sense but impaired higher sense like
stereognosis
• Subcortical
• Impaired primary sense such as vibration and
pinprick but not higher senses
• Internal capsule
• Basal ganglia (globus pallidus and putamen)
• Thalamus
• Face, arm and leg equally involved –
characteristic lesion of the internal capsule
• Dystonic posture- basal ganglia
• Dense sensory loss to pinprick and touch in
the face, arm, leg (thalamic lesion) associated
with hemiplegia (involvement of adjacent internal
capsule)
• Eye deviation and field defect
• Left Brainstem
• Look for crossed hemiplegia – classic feature of
brainstem lesion
• -right hemiplegia from left sided brainstem lesion
often produces left sided brainstem signs (e.g. left sided
dysmetria or cranial nerve palsies at the level of the
lesion)
• Check for cerebellar signs
• -finger to nose test (FTNT) ataxia, alternate pronation
and supination test (APST), heel to toe (tandem gait)
• -limb ataxia is on the same side as the lesion
• Nystagmus (oscillating movement of the eye; slow
component is pathologic because that’s the involuntary
movement)
• -marked when the patient gazes towards the side of
the lesion
• Ipsilateral hearing loss
1 and ½ syndrome. There is L internuclear ophthalmoplegia (A)
with L gaze paresis(B)
Vertical skew deviation in patient with MS( intrinsic brain stem or
cerebellar lesion).
• Sensory findings:
• -pain, temperature and corneal loss on the left side of
the face (involvement of descending tract of V);
• -with pain and temperature loss on right side of the
body (spinothalamic tract)
• Dysarthria and difficulty in swallowing
• -pseudobulbar palsy (usually secondary to multiple
bilateral vascular lesion above the brainstem), also
causes dysarthria and dysphagia
• -with pseudobulbar palsy, there is hyperactive
instead of decreased gag, brisk jaw jerk, emotional lability
and history of previous stroke
• Check for abnormal eye movement
• -example, right hemiplegia secondary to left brain
lesion have trouble gazing to the left or in getting the left
eye to cross the midline when looking to the right
(Internuclear ophthalmoplegia)
• Tongue deviation is to the left with lesion on left 12th
nerve or its nucleus (the stronger right hypoglossus
muscle pushes the tongue to the left ; above the nucleus,
tongue deviates to the right)
 • Eg……
Lateral Medullary (Wallenburg) Syndrome)
• Most common encountered vascular lesion (or syndrome)
affecting the medulla (due to occlusion of ventral or
posterior inferior cerebellar artery).
• Ipsilateral to the lesion – facial numbing, limb ataxia,
Horner’s Syndrome (meiosis, ptosis, anhydrosis), eye
pain.
• Contralateral to lesion - pinprick and temperature loss in
arms and legs, then vertigo nausea, hiccups, hoarseness,
difficulty swallowing, diplopia.
• 7th nerve is not in the medulla.
• 12th or hypoglossal – lesion cause ipsilateral
fasciculation, tongue deviation to the side of the lesion.
• 9th and 10th – dysphagia (laryngeal and pharyngeal
muscles)
• Basic structure of the PONS
• medial involvement cause motor dysfunction,
internuclear opthalmoplagia or gaze palsy to side
lesion.
• lateral involvement – cause pain and temperature
dysfunction.
• vertical nystagmus – sign of brainstem dysfunction at
level of pontomedullary junction or upper midbrain
(unless the patient is on barbiturates).
• 6th n – cochlear and vestibular components.
• trigeminal n. exits from the middle of the pons –
• if involved in this level → produce pain and ipsilateral
loss of corneal reflex.
• high pontine lesion → pain and sensory loss are
contralateral to lesion in both face and extremity.
• below the high pons → pain and temperature senses are
lost ipsilateral in the face and contralateral in limbs.
Pontine(ipsilateral) lesion in MS.There is partial failure of abduction of the right
eye(VI nn. Palsy) associated with b. incomplete facial weakness of the lower
motor neurone type.
 MIDBRAIN
Medial longitudinal fasciculus
lesion result to internuclear opthalmoplagia.
MLF lesion – difficulty in right eye abduction,
nystagmus to abduct-ing left eye when the
patient looks to the left.
Most prominent disturbance in the midbrain
3rd n. nucleus or exiting fibers.
Dilated pupils and opthalmo-plagia.
MS. Bilateral internuclear ophthalmoplegia.
Midbrain lesion just below the superior colliculus produce
difficulty with upward gaze convergence and pupillary
light reflexes (PARINAUD’S SYNDROME)
• Tumors pressing superior colliculus (pinealoma)
• Red Nucleus Lesions
• Contralateral ataxia and tremor (rubral tumors)
• Substancia nigra is located at this level and plays an
important role in PARKINSON’S DISEASE
• 4th n. nucleus is seen in midbrain at lower level and is
seldom involved alone, if involved alone (e.g. – trauma),
4th n. injury causes a head tilt
• Optic Tract fibers concerned with pupillary response
synapse at region of 3rd n. nucleus
• Midbrain lesion may impair pupillary reaction to direct
light but leave contraction to accomodation intact
 Crossings in the CNS
PATHWAY FUNCTION CROSSES INTERPRETATIONS
Pyramidal tract motor Lower medulla Lesion below cross gives ipsilateral
sign
Spinothalamic Pain and On entry to Lesion is always contralateral to pain
tract temp (body) spinal cord and temperature loss (except in the
face)
Spinal tract of 5th Pain and Midpons (runs If lesion is in the medulla or lower
n. temp (face) throughout the pons, there is ipsilateral loss
medulla) If above midpons – there is
contraleteral loss
Spinal dorsal Position and Lower medulla Lesion below crossing gives ipsilateral
column vibration signs

Cerebellar tracts Coordination Crosses 2 Due to “double crossing” lesions of

of movement times (on entry cerebellum or its tracts produce sings
to cerebellum ipsilateral to lesion
and in the
midbrain)

Gaze fibers Coordinates Midpons See eye deviation in neural disease

lateral gaze
CN palsy CN Just above CN Lesion is ipsilateral when CN nuclei is
involved
• Spinal Cord Lesion
• Face is not involved, so are language
and cranial nerves
• Paralysis on the same side of lesion
• -pinprick and temperature loss on
opposite side maybe seen (BROWN-
SEQUARD SYNDROME)
• Sensory level to pinprick or vibration
maybe present
• Bowel and bladder disturbance are
common
Ascending tracts
1. The dorsal column carry position and vibratory sense, fibers rise ipsilateral and
cross in the medulla.
2. Lateral spinothalamic tract – carry pain and temperature sensation, fibers cross
on entering the cord, cord lesions affecting them cause contralateral loss,?
laminate with sacral fibers most laterally placed, therefore expanding lesions in the
center of the cord gives sacral sparing (pinprick and sensory loss to temp are least
prominent in the sacral area).
Descending tracts
3. Lateral corticospinal tract – carry motor fibers, which synapse at anterior horn
cells, fibers, have already crossed in the medulla. Lesion in this area causes weak-
ness, spasticity, and hyperreflexia, upgoing toes?
4. Anterior horn cells – lowers motor neurons, lesion produces weakness, muscle
wasting, fasci-culation, loss of reflex and tone.
5. Anterior spinal artery – supplies the entire cord
except the dorsal column Anterior spinal
syndrome produces paralysis and loss of pain
and temperature sense, position and migratory
sense intact.
• Clinical correlation
• Combined systemic disease affects 1 and 3.
• Amytrophic lateral sclerosis affects 3 and 4.
• Multiple sclerosis affects 1, 2 and 3 (alone or in
combination).
• Poliomyelitis affects 4.
• Brown Sequard syndrome (hemi section of the
cord), ipsilateral paralysis with contraleteral
loss of pinprick.
• Spinal cord
• Sensory level → band of sensory change around thorax
or abdominal or a sharp level below which sensation is
lost
• Distal usually symmetric weakness
• Bowel bladder changes
• PHYSICAL EXAM
• Distal weakness usually worse in the leg then arm, worse
in extensors than flexors
• Tone is increased
• DTR is brisk
• There is BABINSKY sign
• Superficial reflex commonly lost (like anal wink, anal
tone, cremasteric reflex, and abdominal reflex
• Sensory level can be sound
• Root diseases (radiculopathies)
• Hallmark is pain
• Other features are the same as above such
as denervation (weakness, atrophy,
fasciculation) with sensory loss
• Weakness can be proximal
• Radiculopathies of arm commonly involves
C5 and C6 which is proximal, but can be
distal
• Common radiculopathies in the leg involve
the L5 and S1
• Radiculopathy
• Pain is usually severe often described as
sharp, hot or electric and commonly
radiates down an arm or leg
• PHYSICAL EXAM
• Weakness in one myotomal group of
muscles (e.g. C5 and C6 in arm, L5 and S1
in leg, sometimes atrophy and fasciculation)
• Tone is normal or decreased
• DTR? 0 decreased or absent
• Sensory loss to dermatomal distribution
maneuvers may stretch the root eliciting
pain e.g. straight leg raising
• Peripheral neuropathies
• Causes distal, often asymmetric, weakness, with sensory
changes, atrophy and fasciculations may also appear
• HISTORY
• Does the patient wear out his shoes? Catches his toes
and trip (foot drop)? (to test for distal weakness of the
leg)
• Does the patient have trouble with grip or frequently drop
things? (this is a sign of distal strength of the hands)
• Is the process asymmetric? (some are symmetric e.g.
stocking and glove neuropathy, but most are asymmetric
e.g. carpal tunnel syndrome, radial nerve palsy, etc)
• Does the patient notice shrinkage or wasting of muscles
(atrophy) or quivering, twitching (fasciculations)
• Is there numbness, tingling or parasthesia?
CARPAL TUNNEL
SYNDROME
• PHYSICAL EXAM
• Distal often asymmetric weakness with
atrophy, fasciculations, and sensory loss
e.g. decrease pinprick, vibration and
occassionally position sense
• Tone is normal or decreased
• Reflexes are decreased
• Sometimes trophic changes are seen such
as loss of hair and nail and smooth and
shiny skin
• Neuromuscular Junction Disease
• Same as above? But with fatigability, weakness
worsens with use, improves with rest
• Diseased muscles are usually extremely
proximal
• Often involves the muscles of the face (like
drooping of the eye lids, double vision, difficulty
in swallowing or chewing, slurred speech, and
facial weakness.
• PHYSICAL EXAM
• Repetitive test of muscle strength will produce
progressive weakness while rest improves the
strength
• Muscle disease (MYOPATHY)
• proximal muscle weakness, symmetric, without sensory loss
• HISTORY
• Can the patient arise from the chair, get out of a car seat, go
upstairs without using hands? (this is to check proximal
muscle weakness) OR can the patient lift or carry objects? (to
check proximal arm weakness)
• Is weakness relatively symmetric? (minor difference is
allowed since slight asymmetrical weakness may be
observed)
• Is there sensory loss? (pain, cramping and other sensations
may occur with some myopathies but with no sensory loss
• PHYSICAL EXAM
• Proximal symmetric muscle weakness with NO sensory loss
• Tone is normal or slightly decreased
• Reflex is normal or slightly decreased
• Significant atrophy absent except in advanced stage
END OF LECTURE