Neurological Conditions: Bell’s Palsy to Subarachnoid Hemorrhage

Posted on Feb 13, 2026 in Biomedical Sciences

Bell’s Palsy Etiology

Idiopathic; commonly associated with HSV-1, VZV. Autoimmune inflammation or ischemia is suspected. Sporadic outbreaks are reported.

Clinical Features

  • Mastoid/ear pain precedes weakness by 1–2 days.
  • Rapid onset facial weakness within 48 hours.
  • Loss of forehead wrinkling and eye closure.
  • Impaired taste (anterior 2/3 of the tongue).
  • Hyperacusis (stapedius paralysis).
  • Decreased salivation; lacrimation is usually preserved.
  • Bell’s phenomenon (upward/outward eye movement on attempted closure).

Diagnosis

Clinical—sudden unilateral Lower Motor Neuron (LMN) facial palsy. Exclude otitis media, cholesteatoma, stroke, MS, cerebellopontine angle tumours, diabetes, sarcoidosis, and Lyme disease.

Management

  • Eye protection (artificial tears, eye patch/taping).
  • Prednisolone 50–60 mg/day for 7–10 days within 72 hours.
  • Antivirals (acyclovir/valaciclovir) are controversial—consider in severe cases or suspected VZV.
  • Facial physiotherapy to reduce synkinesis.

Prognosis

Good—approximately 70% complete recovery in 4–8 weeks. Incomplete palsy leads to a better outcome. Residual weakness or asymmetry is possible. Aberrant reinnervation can cause synkinesis, jaw-winking, or crocodile tears.

Intervertebral Disc Prolapse

Displacement of disc material leading to compression of the spinal cord or nerve roots.

Age Distribution

  • 30–40 years: most common (hydrated disc).
  • 50–60 years: decreased herniation, increased spinal stenosis, spondylosis, and Osteoarthritis (OA).

Sites

  • Lumbar (most common): L4–L5, L5–S1 → low back pain + sciatica.
  • Cervical: C5–C6, C6–C7 → neck pain radiating to the shoulder, scapula, arm.
  • Thoracic: Rare.

Clinical Features

Back/neck pain, radicular pain, motor weakness, sensory loss, and reflex changes.

Diagnosis

  • Straight leg raise (sensitive).
  • MRI (gold standard): shows disc protrusion + nerve root compression.

Plexitis / Plexopathy

Inflammation or degeneration of a nerve plexus.

Brachial Plexopathy

  • C5–C6 → Erb palsy (shoulder, upper arm weakness).
  • C8–T1 → Klumpke palsy (hand muscle weakness).
  • Causes: trauma, shoulder dislocation, birth injury.

Lumbosacral Plexopathy

Trauma or diabetes → lower limb pain and weakness.

Radiculitis and Radiculopathy

  • Radiculitis: Inflammation of the spinal nerve root.
  • Radiculopathy: Nerve root dysfunction due to compression/irritation.
  • Symptoms: dermatomal pain and/or numbness.

Intracerebral Hemorrhage (ICH)

Etiology Factors

  1. Chronic hypertension, amyloid angiopathy.
  2. Hemorrhagic transformation of ischemic stroke, use of thrombolytics/anticoagulants, arteriovenous malformations (AVMs).

Pathogenesis

Chronic hypertension → Charcot–Bouchard microaneurysms → vessel rupture → hematoma → local ischemia, neuronal death → possible herniation.

Clinical Presentation

  • Non-focal symptoms: Sudden severe headache, vomiting, markedly elevated Blood Pressure (BP).
  • Progression: Rapidly worsening neurological deficits over minutes–hours, contralateral focal signs.
  • Common sites: Putamen (most common), thalamus, cerebellum, pons.

Differential Diagnosis

Hypoglycemia, migraine, seizures, brain tumours, hypertensive encephalopathy.

Diagnosis

  • Gold Standard: Non-contrast CT → hyperdense (bright) hematoma.
  • CT/MR angiography → aneurysm or AVM.
  • Labs: PT, aPTT, INR to assess coagulopathy/anticoagulant use.

Treatment

  • Assess Glasgow Coma Scale (GCS), urgent non-contrast CT.
  • Careful BP reduction to approximately 140 mmHg.
  • Reverse coagulopathy if present.
  • Raised Intracranial Pressure (ICP) → mannitol or hypertonic saline.
  • Large hematoma (>3 cm) or clinical deterioration → surgical evacuation (craniotomy) to reduce ICP and prevent herniation.

Subarachnoid Hemorrhage (SAH)

Collection of blood in the subarachnoid space. Characterized by the “worst headache of my life.”

Etiology (ETI)

  • Trauma.
  • Ruptured saccular (berry) aneurysm.
  • Arteriovenous malformation (AVM).

Risk Factors

Hypertension, smoking, alcohol, cocaine/drug abuse.

Pathogenesis

Rupture of saccular aneurysm at the Circle of Willis bifurcation → arterial blood enters the subarachnoid space → increased ICP and meningeal irritation. Secondary complications include cerebral vasospasm (leading to delayed ischemia), hydrocephalus (from impaired CSF absorption), and rebleeding (highest risk in the first 2 weeks).

Clinical Presentation

  • Non-focal: Sudden severe occipital headache (“worst ever”), vomiting, loss of consciousness (syncope → coma), neck stiffness, photophobia, positive Kernig and Brudzinski signs.
  • Focal: Usually absent initially; may appear later due to vasospasm, intraparenchymal extension, hydrocephalus, or seizures.

Differential Diagnosis

Reversible cerebral vasoconstriction syndrome, cerebral venous sinus thrombosis, cervical artery dissection, intracerebral haemorrhage, meningitis.

Diagnosis

  • Non-contrast CT (within 6 hours): Hyperdensity in sulci, basal cisterns, Sylvian fissures, and/or ventricles.
  • If CT is positive → no lumbar puncture (due to hernia risk).
  • If CT is negative → LP after 12 hours: blood or xanthochromia confirms SAH.
  • Positive CT or CSF → urgent neurosurgical referral.

Treatment

  • ICU admission.
  • BP control: labetalol.
  • Nimodipine 60 mg PO for 21 days to prevent delayed ischemic stroke (vasospasm).
  • HuntHess grade ≤3 → endovascular coiling within 72 hours.
  • Hydrocephalus → external ventricular drain.