After completing this note you will be able to take a focused neurological history, perform a systematic examination, recognise key local aetiologies and outline the immediate and definitive management steps (always verify doses and local protocols against the Kenya MoH guideline and your hospital formulary).
Definition
A structured clinical process that elicits the patient’s symptom chronology, associated systemic features and risk factors, followed by a step‑by‑step neurological examination to localise lesions, grade severity and guide investigations and treatment.
Anatomy and physiology you need
| System | Key structures | Clinical relevance |
|---|---|---|
| Cerebrum | Frontal, parietal, temporal, occipital lobes; motor & sensory cortices | Focal weakness, aphasia, visual field cuts |
| Basal ganglia & thalamus | Caudate, putamen, globus pallidus, thalamic nuclei | Movement disorders, sensory thalamic pain |
| Brainstem | Midbrain, pons, medulla; cranial nerve nuclei | Cranial nerve palsies, respiratory drive |
| Cerebellum | Vermis, hemispheres; Purkinje cells | Ataxia, dysmetria, nystagmus |
| Spinal cord | Cervical, thoracic, lumbar, sacral segments | Level‑specific motor/sensory loss, reflex changes |
| Peripheral nerves & NMJ | Roots, plexi, peripheral nerves, neuromuscular junction | Peripheral neuropathy, myasthenia |
| Meninges & CSF | Dura, arachnoid, pia; CSF dynamics | Headache, meningitis, raised ICP |
Causes and risk factors
- Infectious: HIV (neuro‑candidiasis, CMV, HIV‑associated neurocognitive disorder), cerebral malaria, tuberculous meningitis, bacterial meningitis, neuro‑borreliosis (rare).
- Vascular: Hypertension, diabetes, dyslipidaemia, smoking, sickle‑cell vaso‑occlusion, HIV‑related vasculitis.
- Traumatic: Road‑traffic accidents, falls, assault – common in young males.
- Metabolic: Electrolyte disturbances, renal failure, hepatic encephalopathy, severe malaria‑induced hypoglycaemia.
- Autoimmune / inflammatory: Systemic lupus erythematosus, vasculitis, rheumatic fever (Sydenham’s chorea).
- Neoplastic: Primary CNS tumours (glioma), metastatic disease (breast, lung), Kaposi sarcoma in advanced HIV.
- Nutritional: Vitamin B12 deficiency, thiamine deficiency (Wernicke’s).
- Genetic / congenital: Sickle‑cell disease (stroke risk), neuro‑developmental disorders.
Pathophysiology
Infectious → inflammation → neuronal injury → focal deficits
HIV → immune suppression → opportunistic CNS infection → diffuse or focal lesions
TB meningitis → basal exudates → cranial nerve palsies, hydrocephalus
Cerebral malaria → sequestration of parasitized RBCs → microvascular obstruction → coma, seizures
Sickle‑cell vaso‑occlusion → arterial occlusion → ischemic stroke → motor/sensory loss
Hypertension → arteriolosclerosis → lacunar infarcts → pure motor or sensory syndromes
Autoimmune vasculitis → vessel wall inflammation → ischemia or hemorrhage → multifocal signs
Clinical features
| Domain | Key questions / findings | Why it matters (pathophysiologic link) |
|---|---|---|
| Onset | Sudden vs. insidious; exact time of first symptom | Sudden suggests vascular, trauma or infection; gradual points to neuro‑degeneration, demyelination or metabolic disease |
| Progression | Stepwise deterioration, relapsing‑remitting, continuous decline | Stepwise → demyelinating disease; relapsing‑remitting → multiple sclerosis; continuous → tumour, chronic infection, metabolic encephalopathy |
| Age & gender | Age at presentation, sex | Certain disorders have age peaks (e.g., stroke >55 y, cerebral malaria in children, HIV‑related neuropathy in young adults) |
| Risk factors | Hypertension, diabetes, smoking, HIV status, TB exposure, recent malaria, sickle‑cell crisis, rheumatic fever, family history | Directly point to common Kenyan aetiologies (vascular, infectious, hemoglobinopathies) |
| Focal neurological deficits | Weakness (side, distribution), sensory loss (type, level), visual changes, dysphasia, facial droop | Localisation of lesion to specific CNS region or peripheral nerve |
| Global symptoms | Headache (pattern, triggers), seizures, altered consciousness, fever, neck stiffness | Headache → raised ICP or meningitis; seizures → cortical irritation; fever/neck stiffness → infection |
| Cognitive & behavioural | Memory loss, personality change, hallucinations, mood swings | Diffuse cortical or subcortical involvement (e.g., HIV encephalopathy, TB meningitis, metabolic encephalopathy) |
| Autonomic | Urinary urgency/incontinence, constipation, erectile dysfunction | Spinal cord or brainstem involvement |
| Peripheral signs | Numbness, tingling, burning, gait ataxia, tremor, myoclonus | Peripheral neuropathy (HIV, diabetes, TB drugs), cerebellar disease, extrapyramidal syndromes |
| Systemic review | Recent infections, drug exposures, trauma, travel, vaccinations | Identify precipitating infectious or toxic causes (malaria, TB, antiretroviral neurotoxicity) |
| Functional impact | Ability to perform ADLs, work, school | Guides severity grading and need for urgent intervention |
Examination findings and rationale
- Mental status (alertness, orientation, attention, memory, language) – detects cortical dysfunction, diffuse encephalopathy, or focal lesions.
- Cranial nerves – e.g., CN II visual field defects (optic pathway lesion), CN III‑VI palsy (brainstem or cavernous sinus pathology), CN VII facial weakness (stroke vs. Bell palsy).
- Motor exam – strength grading, tone, bulk; upper motor neuron signs (spasticity, hyperreflexia, Babinski) indicate corticospinal tract disease (stroke, MS, TB meningitis); lower motor neuron signs (flaccidity, fasciculations) point to peripheral neuropathy or anterior horn cell disease.
- Sensory exam – pinprick, vibration, proprioception, cortical modalities; a “stocking‑glove” pattern suggests peripheral neuropathy (HIV, diabetes, antitubercular drugs).
- Coordination – finger‑nose, heel‑shin, rapid alternating movements; dysmetria or ataxia indicates cerebellar or proprioceptive pathway involvement (malaria cerebellitis, cerebellar infarct).
- Gait & stance – hemiplegic gait, spastic gait, ataxic gait, sensory gait; helps localise lesion and assess functional severity.
- Reflexes – deep tendon, plantar, abdominal; hyperreflexia with clonus = UMN lesion; absent reflexes = LMN or peripheral neuropathy.
- Posterior column – Romberg test; instability with eyes closed suggests dorsal column disease (vitamin B12 deficiency, HIV‑related myelopathy).
- Meningeal signs – neck rigidity, Kernig, Brudzinski; positive in meningitis (TB, bacterial, cryptococcal).
- Autonomic testing – bladder scan, perianal sensation; spinal cord compression or cauda equina syndrome.
Differential diagnosis
| Condition | Points toward it | Key discriminators |
|---|---|---|
| Ischaemic stroke | Sudden focal deficit, vascular risk factors, hypertension | Imaging shows territorial infarct; no fever, normal CSF |
| HIV‑associated neurocognitive disorder | HIV+ status, gradual cognitive decline, subcortical signs | CD4 count low, MRI shows diffuse white‑matter changes; improves with ART |
| Tuberculous meningitis | Fever, neck stiffness, recent TB exposure, CSF lymphocytic pleocytosis | CSF low glucose, high protein; MRI basal meningeal enhancement |
| Cerebral malaria | Recent travel to endemic area, fever, seizures, coma | Peripheral smear positive for Plasmodium falciparum; rapid response to antimalarials |
| Sickle‑cell vaso‑occlusive CNS crisis | Sickle‑cell disease, acute pain crisis, focal deficits | MRI shows diffusion restriction in watershed zones; resolves with transfusion |
| Rheumatic chorea | Recent streptococcal infection, choreiform movements, young female | Positive ASO titre, resolves with anti‑inflammatory therapy |
| Multiple sclerosis | Relapsing‑remitting course, optic neuritis, sensory level, young adult | MRI shows periventricular plaques, oligoclonal bands in CSF |
| Peripheral neuropathy (HIV, TB drugs) | Distal symmetric numbness, stocking‑glove, drug history | Nerve conduction studies show demyelination or axonal loss; improves on drug cessation |
| Brain tumour (glioma, metastasis) | Progressive headache, focal signs, seizures, weight loss | MRI with contrast shows mass effect; biopsy confirms histology |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Non‑contrast CT head | Acute bleed, mass effect, hydrocephalus | Hyperdense area = haemorrhage; hypodense = infarct >24 h |
| MRI brain with contrast | Detailed lesion localisation, demyelination, infection | T2/FLAIR hyperintensity = oedema/inflammation; ring‑enhancing lesion = abscess or tumour |
| Lumbar puncture (CSF analysis) | Infectious vs. inflammatory vs. neoplastic processes | High neutrophils = bacterial meningitis; lymphocytes + low glucose = TB meningitis; oligoclonal bands = MS |
| Full blood count & ESR/CRP | Inflammation, infection, anaemia | Elevated ESR/CRP supports TB or systemic infection |
| HIV serology & CD4 count | Immunosuppression level | CD4 <200 cells/µL raises risk of opportunistic CNS infections |
| Blood glucose & electrolytes | Metabolic encephalopathy | Hyper/hypoglycaemia, hyponatraemia explain altered mental status |
| Serum vitamin B12 & folate | Nutritional neuropathy | Low B12 → subacute combined degeneration |
| Nerve conduction studies / EMG | Peripheral nerve vs. muscle disease | Reduced conduction velocity = demyelinating neuropathy; reduced amplitude = axonal loss |
| Chest X‑ray | Pulmonary TB, sarcoidosis | Upper lobe infiltrates = TB; hilar lymphadenopathy = sarcoid |
| Malaria rapid diagnostic test / thick smear | Current malaria infection | Positive parasite confirms malaria‑related CNS disease |
| Sickle‑cell screen (Hb electrophoresis) | Confirm sickle‑cell disease | HbS >40 % confirms diagnosis |
Diagnosis and severity
| Clinical syndrome | Diagnostic criteria (snapshot) | Severity grading (examples) |
|---|---|---|
| Acute ischaemic stroke | Sudden focal deficit + imaging evidence of infarct | NIH Stroke Scale: mild (0‑5), moderate (6‑15), severe (>15) |
| TB meningitis | Subacute meningitic picture + CSF lymphocytosis, low glucose, high protein + MRI basal enhancement | British Medical Research Council stages: Stage I (alert), Stage II (confused), Stage III (coma) |
| HIV‑associated neurocognitive disorder | HIV+ + neurocognitive testing showing impairment + exclusion of other causes | Asymptomatic neurocognitive impairment, mild neurocognitive disorder, HIV‑associated dementia |
| Cerebral malaria | Recent travel, fever, seizures + peripheral smear positive for P. falciparum | WHO coma score: mild (≥11), moderate (8‑10), severe (≤7) |
| Sickle‑cell CNS crisis | Sickle‑cell disease + acute focal deficit during vaso‑occlusive episode + MRI diffusion restriction | Mild (single transient deficit), moderate (persistent deficit <1 week), severe (deficit >1 week or coma) |
| Peripheral neuropathy (drug‑induced) | Distal symmetric sensory loss + nerve conduction study showing axonal loss + temporal relation to drug | Graded by NCI‑CTCAE: Grade 1 (asymptomatic), Grade 2 (moderate symptoms), Grade 3 (severe limiting ADL) |
| Brain tumour | Progressive focal signs + contrast‑enhancing mass on MRI + histology (if biopsied) | WHO tumour grade I‑IV; functional status by Karnofsky Performance Scale |
Severity guides urgency of imaging, need for intensive monitoring, and choice of definitive therapy.
Management
Immediate stabilisation
- Airway, Breathing, Circulation – protect airway if reduced consciousness (GCS < 8) and consider end‑tidal CO₂ monitoring; give supplemental O₂ to keep SpO₂ > 94 %.
- Glucose – check capillary glucose; treat hypoglycaemia with IV dextrose (or glucagon if IV unavailable).
- Seizure control – if ongoing seizure, give a rapid‑acting benzodiazepine (e.g., lorazepam) intravenously; follow with a longer‑acting antiepileptic (e.g., phenytoin, valproate) to prevent recurrence.
- ICP‑raising lesions – elevate head of bed 30°, avoid neck flexion, give osmotic agents (mannitol or hypertonic saline) if signs of herniation.
- Hypertensive emergency with neurological deficit – lower mean arterial pressure by 15 % within the first hour using IV labetalol or nicardipine; avoid rapid over‑correction.
Definitive treatment – directed at the underlying aetiology
| Condition | First‑line drug class | Rationale |
|---|---|---|
| Bacterial meningitis | Third‑generation cephalosporin + vancomycin | Broad coverage for common pathogens and resistant Streptococcus pneumoniae |
| Tuberculous meningitis | Anti‑TB regimen (rifampicin, isoniazid, pyrazinamide, ethambutol) + adjunctive steroids | Steroids reduce mortality and neurologic sequelae |
| Cerebral malaria | Artemisinin‑based combination therapy | Rapid parasite clearance; prevents cerebral oedema |
| HIV‑related opportunistic CNS infection | Appropriate antiretroviral + pathogen‑specific therapy (e.g., cryptococcal fluconazole) | Immune restoration plus targeted antimicrobial |
| Stroke (ischemic) | Antiplatelet (aspirin) ± anticoagulation if cardio‑embolic | Prevents extension of infarct |
| Stroke (hemorrhagic) | Blood pressure control, reversal of anticoagulation, neurosurgical evacuation if indicated | Limits expansion of bleed |
| Guillain‑Barré syndrome | IV immunoglobulin or plasma exchange | Modulates immune attack on peripheral nerves |
| Sickle‑cell vaso‑occlusive CNS crisis | Exchange transfusion, analgesia, hydration | Reduces HbS concentration, improves oxygen delivery |
Monitoring & follow‑up
- Neurological status every 15 min for the first hour, then hourly (GCS, pupil size, motor response).
- Vital signs, fluid balance, electrolytes, and glucose at least every 4 h.
- Repeat imaging (CT/MRI) if deterioration or after 24–48 h for stroke/TB meningitis.
- For infections, monitor CSF parameters, culture results, and drug toxicities (e.g., renal function with aminoglycosides).
- Rehabilitation referral early for stroke, GBS, or traumatic brain injury.
Contra‑indications & safety
- Avoid nitroprusside in raised ICP (can increase cerebral blood flow).
- Do not give fibrinolysis in intracerebral haemorrhage or recent major surgery.
- Steroids are contraindicated in viral encephalitis (except HSV where they may be used adjunctively).
- Ensure correct positioning of lumbar puncture needle to avoid spinal cord injury; defer LP if signs of raised ICP without prior imaging.
Complications and prognosis
- Secondary brain injury – cerebral oedema, herniation, seizures; early control of ICP and seizures improves outcome.
- Infection‑related sequelae – hydrocephalus after meningitis, tuberculoma formation; may need shunting or prolonged antimicrobial therapy.
- Vascular complications – hemorrhagic transformation of ischemic stroke, arterial dissection; monitor with serial imaging.
- Functional deficits – motor weakness, aphasia, visual field loss; prognosis depends on lesion size, speed of reperfusion, and comorbidities (e.g., HIV, sickle cell).
- Neurocognitive decline – common after severe malaria or HIV encephalopathy; requires neuro‑rehab and psychosocial support.
Overall mortality is highest for TB meningitis, cerebral malaria, and large‑territory strokes; early stabilisation and disease‑specific therapy markedly improve survival and reduce long‑term disability.
High‑yield exam points
- Look‑alike conditions:
- TB meningitis vs. cryptococcal meningitis – CSF opening pressure very high in cryptococcal; India‑ink positive.
- Ischaemic stroke vs. seizure‑postictal deficit – stroke shows diffusion restriction on MRI; post‑ictal deficits resolve within minutes‑hours.
- Common wrong first step: Performing a lumbar puncture before CT in a patient with focal deficit or papilledema – risk of herniation.
- Examiner bedside questions:
- “What three signs would make you suspect raised intracranial pressure?” (Papilledema, Cushing’s triad, abnormal posturing)
- “How would you differentiate an upper motor neuron from a lower motor neuron lesion on exam?” (Spasticity, hyperreflexia, Babinski vs. flaccidity, fasciculations, atrophy)
- “If a patient with suspected meningitis is allergic to penicillin, what alternative regimen would you choose?” (Third‑generation cephalosporin plus vancomycin, or chloramphenicol in resource‑limited settings).
Clinical case
Case: A 28‑year‑old male with known sickle cell disease presents with sudden onset left‑sided weakness and headache. He is febrile (38.5 °C), GCS 15, pupils equal, fundi show papilledema. CT head shows a right parietal hypodense area with surrounding edema.
Questions
- What is the most likely diagnosis?
Answer: Acute sickle‑cell vaso‑occlusive cerebral infarct with cerebral oedema.
- What immediate management step is mandatory before any further imaging?
Answer: Secure airway if mental status declines, give supplemental O₂, and start IV fluids (isotonic, avoiding overload) while arranging urgent exchange transfusion to reduce HbS.
- Which long‑term therapy reduces recurrence of similar events in this patient?
Answer: Chronic hydroxyurea therapy to increase fetal haemoglobin and reduce sickling episodes, combined with regular transfusion program if indicated.
Practice questions
Question 1
A 45‑year‑old woman with HIV presents with fever, neck stiffness, and a GCS of 13. CT brain is normal. What is the next best step?
A. Start high‑dose steroids
B. Perform lumbar puncture
C. Give IV ceftriaxone only
D. Order MRI brain
Answer: B. Perform lumbar puncture
Explanation: In the absence of radiological signs of raised ICP, LP is essential to obtain CSF for diagnosis and to start targeted antimicrobial therapy.
Question 2
A child from a malaria‑endemic area is comatose, with a peripheral smear showing Plasmodium falciparum parasites. Which adjunctive therapy improves outcome?
A. High‑dose vitamin C
B. Mannitol
C. Artesunate‑based combination therapy
D. Broad‑spectrum antibiotics
Answer: C. Artesunate‑based combination therapy
Explanation: Rapid parasite clearance with artemisinin derivatives reduces cerebral oedema and mortality in cerebral malaria.
Question 3
A 60‑year‑old man with atrial fibrillation on warfarin presents with right‑sided weakness. CT shows a left middle‑cerebral‑artery infarct with no haemorrhage. Which medication is contraindicated?
A. Aspirin
B. Low‑molecular‑weight heparin
C. Tissue‑plasminogen activator (tPA)
D. Statin
Answer: C. Tissue‑plasminogen activator (tPA)
Explanation: Recent anticoagulation with warfarin (INR > 1.7) is an absolute contraindication to thrombolysis due to bleeding risk.
Question 4
A patient with suspected Guillain‑Barré syndrome shows progressive ascending weakness. Which investigation result would push you toward an alternative diagnosis?
A. Albumin‑cytologic dissociation in CSF
B. Nerve‑conduction studies showing demyelination
C. Elevated CSF protein with normal cell count
D. Presence of anti‑GM1 antibodies
Answer: D. Presence of anti‑GM1 antibodies
Explanation: Anti‑GM1 antibodies suggest a variant of GBS (acute motor axonal neuropathy) but do not exclude GBS; however, a markedly high CSF white cell count would point to infection rather than GBS.
Question 5
A 30‑year‑old male with newly diagnosed TB meningitis is started on standard anti‑TB drugs and steroids. Which monitoring parameter is most critical in the first week?
A. Serum calcium
B. Liver function tests
C. Visual acuity
D. Serum potassium
Answer: B. Liver function tests
Explanation: First‑line anti‑TB drugs are hepatotoxic; early detection of transaminitis guides dose adjustment or drug substitution.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.