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Pathology affecting the upper motor neurone tends to produce spastic paralysis- i.e. stiff,
weak limbs. However, in the early stages, the affected limbs may be flaccid.
Pathology affecting the lower motor neurone tends to produce flaccid paralysis- i.e. floppy,
weak limbs. The muscles affected become atrophied, with visible loss of bulk.
Lesions in the brain are more likely to produce focal motor neurology (often a hemiplegia
paralysing the arm extensors and leg flexors on the contralateral side. There may be
associated symptoms and signs of raised intracranial pressure. Some lesions are associated
with seizures (which may be focal). Lesions in the brain are also more likely to interfere with
conscious level/ higher mental function.
Lesions affecting the spinal cord are more likely to produce symmetrical paralysis below the
level of the lesion, with sensory loss. There also may be associated sphincter dysfunction
affecting bowel and bladder control.
In lesions affecting peripheral nerves the distal muscle groups are often affected first.
In myopathic paralysis, the pattern of paralysis is determined by affected muscles. There
may be muscle wasting, pseudohypertrophy (suggests DMD) or tenderness.
Causes of paralysis: (rare diagnoses in brackets))
1. Cerebral pathology
Head injury
Cerebrovascular accidents- due to vascular malformations, sickle cell disease,
bleeding tendency, thrombosis, emboli eg rheumatic heart disease, HIV
Infection- meningitis, cerebral abscess, subdural empyema, sequelae of cerebral
malaria, TB tuberculoma, toxoplasmosis
HIV: encephalitis/ focal inflammation; opportunistic infections eg. CMV
Tumour- benign or malignant
Cerebral Palsy -new neurological signs appear as child develops
Migraine
Todds palsy post seizure
2. Spinal cord pathology
Trauma
Transverse Myelitis, including HIV-related
Epidural abscess
Schistosomiasis
TB spine
Paravertebral tumours eg. Burkitts lymphoma
(Cysticercosis)
(Poliomyelitis)
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3. Peripheral Neuropathies
Guillain-Barre Syndrome (GBS)
HIV-related polyneuropathies- direct HIV-effect; or co-infections e.g. CMV
Rabies (flaccid form)
(Diphtheria)
(Botulism)
(Tick Paralysis)
4. Muscle pathology
Acute viral myositis
(Myasthenia Gravis crisis)
5. Miscellaneous
Organophosphate poisoning (rare presentation of chronic poisoning)
(Vitamin B deficiencies)
Common Causes of Non-traumatic Paraplegia in Malawi
Burkitts Lymphoma
Spinal TB
Epidural abscess
Guillain Barre Syndrome
Transverse Myelitis
Schistosomiasis often asymmetrical
Polio not common but must be excluded
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Investigations
Treatment
Specific treatments depend on cause identified or suspected.
Meningitis: Broad-spectrum antibiotics, preferably after LP
Cerebral or spinal abscess: Ceftriaxone and seek surgical opinion.
TB spine or tuberculoma: TB treatment and orthopaedic opinion
Schistosomiasis- Praziquantel, 40 mg/kg stat (consider this whenever no other cause
for paralysis found and in ALL cases of paraparesis).
Consider steroids for ALL spinal cord lesions
Tumours: treat with surgery/ chemotherapy if appropriate. Palliative care.
Organophosphate poisoning- see poisoning protocol
Thrombotic disease- prophylactic aspirin
Supportive Care
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Monitoring
Regular BP, vital signs, saturation (especially children with GBS), neuro signs
Regular documentation of level of disorder in ascending polyneuropathies such as
Guillain-Barre syndrome. Peak expiratory flow monitoring can be a useful way to
assess decline of respiratory function.
Regular check for pressure sores
Complications
When to discharge
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Non-communicating:
o Congenital malformation (especially aqueduct stenosis), may be associated
with spina bifida (Chiari malformation); vascular malformation.
o Neoplastic Tumour
Communicating:
o Infection: Secondary to meningitis, intrauterine infection.
o Post haemorrhagic Premature infants with IVH, post subdural/subarachnoid
haemorrhage.
o Dural venous sinus thrombosis
Investigation:
Cranial USS.
Consider ventricular tap if signs of infection / raised ICP
Management:
Therapeutic ventricular tap if signs acute raised ICP
Surgical referral for ventriculo-peritoneal shunt.
Complications of VP shunts:
Shunts can become infected or blocked and need to be treated urgently.
Suspect in a child with VP shunt if any of:
Vomiting
Headache
Reduced level of consciousness
Ataxia
Cranial nerve palsy
Visual disturbance
Investigation of possibly blocked shunts:
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Meningitis
When to suspect Meningitis
In any child with fever and meningism (vomiting, neck stiffness, headache,
photophobia, etc)
In any infant presenting with fever, poor feeding, bulging fontanelle or irritability
In any infant / child with fever and convulsions and no other obvious cause is found.
In a child in whom it is difficult to rule out meningitis, especially in young infants and
neonates who may present with subtle, non-specific signs e.g. not feeding, lethargy,
irritability, jaundice or apnoeic episodes.
Any child aged 2 months and above with hazy CSF or a positive CSF
microscopy should be admitted to the Research Ward.
Treatment
Resuscitation
ABC
Correct shock and dehydration
Correct hypoglycaemia
Stop seizures (see protocol)
Antibiotics
Health centre - follow IMCI guidelines Very Severe Febrile Disease
In Hospital
x 14 - 21 days
OR
Ceftriaxone 50mg / kg o.d x 10 days (discuss with Consultant)
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Try to keep the IV treatment for at least 48 hours AND as long as possible; but im
antibiotics can then be used.
Give all antibiotics parenterally.
Switch to appropriate antibiotics as soon as culture & sensitivities are known.
Steroids are NOT necessary
*Salmonella Meningitis
Salmonella meningitis should be treated for at least 14 days with ceftriaxone followed
by Ciprofloxacin 10mg / kg / dose / bd PO for 14 days (on discharge).
Supportive Management
Fluids / Nutritional Support
Give maintenance fluids once shock and dehydration have been corrected (IV initially
or later by NGT), unless taking fluid well by mouth
Avoid over hydration by careful fluid balance and in particular avoid IV fluids
with low sodium levels e.g. 5% dextrose.
Use 0.9%NS with added glucose to make 10% dextrose for infants and those
children with hypoglycaemia (see fluids p69)
If still unable to tolerate fluids by mouth after 36 - 48 hours
o pass an NG tube
o give boluses of milk / sugar solution
Blood Sugar
Check blood glucose
o on all children on presentation
o on any child who starts fitting
o deteriorating conscious level
If blood sugar < 2 mmol/ l (2.2 if glucometer available)
o give 1ml/kg 50% dextrose iv stat slowly
o consider NGT feeds
Recheck blood glucose after 30 minutes. If it remains low, repeat the IV glucose and
continue monitoring. Consider a continuous infusion or NGT feeds if not already in
place
Oxygen
Give when necessary e.g. when SaO2 < 90%, child cyanosed, or in respiratory
distress
Hyperpyrexia
Most children will need paracetamol for fever and pain relief
o Give 30mg / kg PR loading dose or
o 20mg /kg PO loading dose
o 15mg /kg maintenance doses qds
Convulsions
See Seizure protocol p25
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Monitoring
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