Neurology

Question 1

First line drug for peripheral neuropathy?

Answer 1

Amitriptyline

(Second line: Duloxetine, gabapentin pregabalin)

If oral therapy not accepted, trial capsaisin.

Question 2

What nerves control the following reflexes?

Biceps
Supinator
Triceps

Knee jerk
Ankle

Answer 2

Biceps-Musculocutaneous (C5)
Supinator - Radial (C6)
Triceps- Radial (C6)

Knee jerk- Femoral nerve (L3)
Ankle- Tibial nerve (S1)

Question 3

What is the site of the lesion in upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 3

UMN: Cerebral hemispheres, cerebellum, brainstem, or spinal cord.

LMN: Anterior horn cell, motor nerve roots, or peripheral motor nerves.

Question 4

Q: What are the inspection findings in upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 4

UMN: No fasciculations or significant wasting (though there may be some disuse atrophy or contractures).

LMN: Wasting and fasciculation of muscles.

Question 5

Q: How does tone present in upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 5

UMN: Increased tone (spasticity or rigidity) +/- ankle clonus.

LMN: Decreased tone (hypotonia, flaccid) or normal.

Question 6

How does power present in upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 6

UMN: Reduced power with a pyramidal pattern of weakness (extensors weaker than flexors in arms, flexors weaker than extensors in legs).

LMN: Reduced power in the distribution of the affected motor root or nerve.

Question 7

How do reflexes present in upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 7

UMN: Exaggerated or brisk reflexes (hyperreflexia).

LMN: Reduced or absent reflexes (hyporeflexia or areflexia).

Question 8

What is the plantar reflex in upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 8

UMN: Upgoing/extensor (Babinski positive).

LMN: Downgoing/flexor or no movement.

Question 9

Q: What are some examples of conditions caused by upper motor neuron (UMN) and lower motor neuron (LMN) lesions?

Answer 9

UMN:
Ischaemic or haemorrhagic stroke (including brainstem strokes).
Amyotrophic lateral sclerosis (ALS).
Multiple sclerosis (MS).

LMN:
Peripheral nerve trauma/compression.
Spinal muscular atrophy.
Amyotrophic lateral sclerosis (ALS).
Guillain-Barré syndrome.
Poliomyelitis.

Question 10

What is Motor Neuron Disease (MND), and what causes it?

Answer 10

MND is a progressive neuromuscular disorder caused by the death of motor neurons in the brain, brainstem, and spinal cord.

It results in muscular limb and bulbar weakness.

The sensory system and cranial nerves to the eye muscles are not involved.

5-10% of cases are inherited (autosomal dominant), while the rest are sporadic.

Question 11

What are the three main patterns of Motor Neuron Disease (MND)?

Answer 11

Amyotrophic lateral sclerosis (ALS/Lou Gehrig disease):
- Combined LMN muscle atrophy and UMN hyper-reflexia, leading to progressive spasticity.
- Most common type.

Progressive muscle atrophy:
- Wasting begins in distal muscles with widespread fasciculation.
- Progressive bulbar palsy (LMN) and pseudobulbar palsy (UMN):

LMN lesions in the brainstem motor nuclei.
- Results in a wasted, fibrillating tongue, weakness of chewing, swallowing, and facial muscles.

Question 12

What are the key symptoms and signs of Motor Neuron Disease (MND)?

Answer 12

Weakness or muscle wasting (first noticed in hands or feet).

Stumbling (spastic gait, foot drop).

Difficulty with swallowing and speech (slurring, hoarseness).

Fasciculation (twitching) of skeletal muscles and fibrillating tongue.

Cramps, emotional instability, depression, and ± muscle pain.

Question 13

How is Motor Neuron Disease (MND) diagnosed and managed?

Answer 13

Diagnosis:

Clinical diagnosis (no specific diagnostic tests).

Neurophysiological tests and MRI of the brain/spinal cord help differentiate from other conditions.

Management:

Incurable; progresses to death within 3-5 years (due to ventilatory failure/aspiration pneumonia).

Riluzole (sodium channel blocker) may slightly slow progression.

Baclofen for cramps, botulinum toxin for spasticity, and propantheline/amitriptyline for drooling.

Multidisciplinary care is essential.

Question 14

Eye muscles supplied by which cranial nerves?

Answer 14

(LR6, SO4) 3
6 Abducencs
4 trochlear
3 occulomotor

Question 15

What is the difference between simple partial and complex partial seizures?

Answer 15

Both focal onset (partial)
Simple - Aware
Complex- Impaired awareness

Question 16

Q: What are the key features of complex partial seizures (temporal lobe epilepsy)?

Answer 16

Commonest manifestation: Slight disturbance of perception and consciousness.

Hallucinations: Visual, taste, smell, or sounds.

Affective feelings: Fear, anxiety, anger.

Dyscognitive effects: Deja vu, jamais vu, waves emanating from the epigastrium.

Objective signs: Lip-smacking, swallowing/chewing/sucking, unresponsiveness, pacing.

Memory loss: Permanent short-term memory loss may occur.

Question 17

What are the key features of simple partial seizures (Jacksonian epilepsy)?

Answer 17

No loss of consciousness.

Focal seizures: Jerking movements begin at the angle of the mouth, thumb, or index finger and “march” to involve the rest of the body (e.g., thumb → hand → limb → face ± leg).

May progress to a generalised tonic-clonic seizure or complex partial seizure.

Question 18

What are the key features of absence seizures?

Answer 18

Typical age group: Children aged 4 years to puberty.

Key features:

Child suddenly stops activity and stares.

Motionless (may blink or nod).

No warning.

May have clonic (jerky) movements of eyelids, face, or fingers.

Lip-smacking or chewing (complex absence).

Lasts 5-10 seconds; child resumes activity as if nothing happened.

May occur several times per day.

Diagnosis:

EEG: Classic 3 Hz wave and spike pattern.

Hyperventilation or sleep deprivation can help evoke seizures.

Question 19

What is narcolepsy, and what are its key features?

Answer 19

Narcolepsy: A permanent neurological disorder characterized by irresistible daytime sleep attacks.

Key features (tetrad of symptoms):

Daytime hypersomnolence: Sudden, brief sleep attacks (15-20 minutes).

Cataplexy: Sudden loss of muscle tone triggered by surprise or emotional upset.

Sleep paralysis: Inability to move while drowsy (between sleep and waking).

Hypnagogic/hypnopompic hallucinations: Terrifying hallucinations when falling asleep or waking up.

Diagnosis:

Clinical history.

EEG monitoring and sleep laboratory studies (e.g., sleep latency test with rapid eye movement as a hallmark).

Question 20

What is the management approach for a first-ever tonic-clonic seizure?

Answer 20

1. Investigate the cause (e.g., EEG, imaging).
   2.Treat the cause if possible.
2. Assess recurrence risk and patient preference for treatment:
   - If high recurrence risk or patient prefers treatment:
   –Focal (partial) seizure: Start carbamazepine.
   –Generalised seizure: Start sodium valproate.
   -If low recurrence risk or patient prefers observation: Monitor without treatment.

Question 21

What are the two main types of epilepsy based on onset, and what are their subtypes?

Answer 21

1. Focal onset (partial):
   - Aware (simple partial): No loss of consciousness.
   - Impaired consciousness. Focal to bilateral tonic-clonic (secondarily generalised tonic-clonic).
2. Generalised onset:
   Motor:
   Tonic-clonic.
   Tonic.
   Myoclonic.

Nonmotor:
Absence.

Question 22

A patient presents with a one-sided, pulsating headache lasting 4-72 hours, aggravated by physical activity, and associated with nausea, photophobia, and phonophobia. What is the likely diagnosis?

Answer 22

Migraine.

Duration: 4 to 72 hours.
Location: Typically one-sided (not side-locked, can be bilateral).
Quality: Pulsating, moderate to severe intensity.
Aggravating factors: Routine physical activity.
Associated symptoms: Nausea, photophobia, phonophobia, or osmophobia.
Aura: May or may not be present (reversible focal neurological symptoms lasting <60 minutes).

Question 23

A patient reports reversible focal neurological symptoms (e.g., visual disturbances, sensory changes) lasting 5-20 minutes, followed by a pulsating headache with nausea and photophobia. What is the likely diagnosis?

Answer 23

Migraine with aura.

Aura: Reversible focal neurological symptoms (e.g., visual, sensory, speech/language, motor, brainstem, or retinal) that develop over 5-20 minutes and last <60 minutes.

Headache: Follows aura, with typical migraine features (pulsating, one-sided, nausea, photophobia, etc.).

Differential diagnosis: Must exclude transient ischaemic attack (TIA).

Question 24

A patient describes scintillating scotoma (visual aura) but no headache follows. What is the likely diagnosis?

Answer 24

Aura without headache (acephalgic migraine)

Definition: Typical migraine aura without an accompanying headache.

Common form: Scintillating scotoma (visual aura).

Diagnosis: Must exclude aura mimics, especially transient ischaemic attack (TIA).

Question 25

A patient has a bilateral headache lasting 30 minutes to 7 days, described as pressure or tightness, with no nausea but possible photophobia or phonophobia. What is the likely diagnosis?

Answer 25

Tension-type headache. Duration: 30 minutes to 7 days. Location: Bilateral, feels like pressure or tightness. Intensity: Mild to moderate (rarely severe). Associated symptoms: No nausea, but may have photophobia or phonophobia. Diagnosis: Does not fit criteria for other headache types better than tension-type headache.

Question 26

A patient presents with a unilateral, side-locked headache associated with tearing, conjunctival injection, and nasal stuffiness. They are also agitated and restless. What is the likely diagnosis?

Answer 26

Trigeminal autonomic cephalgias (TACs) Location: Unilateral and side-locked (follows the first division of the trigeminal nerve). Autonomic features: Tearing, conjunctival injection, ptosis, nasal stuffiness, facial flushing, or sweating. Associated symptoms: Possible photophobia or phonophobia (usually unilateral). Patient behavior: Often agitated and restless.

Question 27

A patient reports a thunderclap headache triggered by exertion or sexual activity, with fluctuating neurological deficits and seizures. Imaging shows a "string and bead" appearance on angiography. What is the likely diagnosis?

Answer 27

Reversible cerebral vasoconstriction syndrome (RCVS). Onset: Thunderclap headache, recurring over 1-2 weeks. Triggers: Exertion, Valsalva manoeuvre, sexual activity, strong emotion, postpartum, or serotonergic/sympathomimetic drugs. Associated symptoms: Fluctuating neurological deficits, seizures. Imaging: Angiography shows "string and bead" appearance but may be normal in first week; MRI may show posterior oedema, infarction, or haemorrhage.

Question 28

A patient has had a daily headache since a specific onset date, lasting >3 months, with no specific features. What is the likely diagnosis?

Answer 28

New daily persistent headache (NDPH) Definition: Persistent and daily headache since onset (patient remembers starting date), present for >3 months. Characteristics: No specific features (may resemble migraine or tension-type headache). Management: Treat based on the main phenotype (e.g., migraine or tension-type headache).

Question 29

A patient experiences a sudden, severe headache during or after sexual activity, which resolves spontaneously over a few months. What is the likely diagnosis?

Answer 29

Primary headache associated with sexual activity (benign sex headache). Timing: Occurs before (milder) or at (more abrupt and severe) orgasm. Duration: Often resolves spontaneously over a few months. Differential diagnosis: Must exclude reversible cerebral vasoconstriction syndrome (RCVS) and subarachnoid haemorrhage.

Question 30

A patient develops a headache after strenuous exercise, especially in hot weather or at high altitude, lasting <48 hours. What is the likely diagnosis?

Answer 30

Primary exercise headache (benign exertional headache) Trigger: Strenuous physical activity, especially in hot weather or at high altitude. Duration: Lasts <48 hours. Differential diagnosis: Exclude space-occupying lesions, aneurysm, carotid stenosis, or posterior fossa mass lesions. May be an unusual presentation of angina

Question 31

A patient describes brief, stabbing pains in the head lasting a few seconds, occurring irregularly and without autonomic features. What is the likely diagnosis?

Answer 31

Primary stabbing headache (ice-pick headache). Occurs spontaneously in the absence of organic disease. May occur with migraines. Description: Transient, localised stabs of pain in the head. Duration: Each stab lasts a few seconds; stabs recur irregularly. Location: Mainly extratrigeminal, but can change site. Management: No treatment needed for isolated cases; persistent cases may respond to indomethacin.

Question 32

A patient reports a headache triggered by coughing or Valsalva manoeuvre, lasting seconds to 2 hours. What is the likely diagnosis?

Answer 32

Primary cough headache (benign cough headache). Provoked by: Cough or Valsalva manoeuvre. Duration: Lasts seconds to 2 hours. Differential diagnosis: Exclude space-occupying lesions, aneurysm, posterior fossa pathology, Chiari malformation, and cerebrospinal fluid obstruction.

Question 33

An older patient is woken at 1-3 am by a bilateral headache lasting 30-60 minutes, often prevented by coffee before bed. What is the likely diagnosis?

Answer 33

Hypnic headache. Typical patient: Older (more than 50 years). Timing: Woken early (1 to 3 am) by bilateral headache, often with nausea. Duration: Usually lasts 30 to 60 minutes (up to 4 hours). Prevention: Often prevented by 1-2 cups of coffee before bed. Treatment: Lithium, melatonin, and indomethacin may also be used. Hypnic headache may be confused with exploding head syndrome (a parasomnia), in which a patient wakes from sleep shortly after onset with sense of a loud bang (painless) in the head. May respond to 1 to 2 cups of coffee before bed.

Question 34

A patient has a headache that is worse in the evening, improves when lying flat, and is associated with "coat-hanger" pain across the shoulders. What is the likely diagnosis?

Answer 34

Low cerebrospinal fluid (CSF) pressure headache. Low Cerebrospinal Fluid (CSF) Pressure Headache Timing: Generally worse in the evening and improved by lying flat. Associated symptoms: "Coat-hanger" pain across the shoulders. Pulsatile tinnitus. Intracranial pressure: Less than 6 cmH₂O. Causes: May be spontaneous or follow trauma or dural puncture. Treatment post lumbar puncture headache: Strict bed rest, paracetamol + codeine PRN, Rehydrate, review in 24h, explain post lumbar puncture headache usually resolves in 24 hours

Question 35

A patient presents with a headache that is worse in the morning and when lying down, improved by upright posture, and associated with pulsatile tinnitus and papilloedema. What is the likely diagnosis?

Answer 35

Increased cerebrospinal fluid (CSF) pressure headache. Associated with: Raised intracranial pressure (more than 25 cmH₂O, measured by lumbar puncture manometry in the lateral decubitus position). Timing: Typically worse in the morning and when lying down, improved by upright posture. Aggravating factors: Cough, straining, and Valsalva manoeuvre. Associated symptoms: Transient visual obscuration. Pulsatile tinnitus. Papilloedema. Exclude space-occupying lesions, venous sinus thrombosis, obstruction, and drugs such as tetracyclines (eg doxycyline) and vitamin A analogues (e.g., isotretinoin, acitretin). Consider: Idiopathic intracranial hypertension (pseudotumor cerebri), especially if there is recent weight gain. - Tx- stop tetracyclines, refer urgently to neuro / ED, acetazolamide under specialist care Complications: Visual field loss and permanent damage can follow initial transient visual problems.

Question 36

A patient has a unilateral headache radiating from the posterior to anterior head, associated with neck pain and reduced neck range of motion. What is the likely diagnosis?

Answer 36

Cervicogenic headache. Associated symptoms: Neck pain. Unilateral headache (side-locked) with radiations from posterior to anterior. Cause: Due to a disorder of the cervical spine (e.g., bone, disc, soft tissue). Examination findings: Reduced range of neck movement. Headache is provoked by neck manoeuvres or digital pressure on affected structures. Treatment: High cervical or greater occipital nerve block may relieve symptoms.

Question 37

A patient develops a headache after taking drugs such as alcohol, nitrates, or phosphodiesterase inhibitors. What is the likely diagnosis?

Answer 37

Drug-induced headache. Triggered by: Intake of drugs such as: Alcohol, marijuana, cocaine, monosodium glutamate, nitrates, cyclosporine, phosphodiesterase inhibitors, carbon monoxide, exogenous hormones.

Question 38

A patient with obstructive sleep apnoea or hypertension presents with a headache. What is the likely diagnosis?

Answer 38

Headache induced by metabolic/other medical condition. Associated with: A medical condition such as: Obstructive sleep apnoea, hypoxia, arterial hypertension, phaeochromocytoma, epilepsy, hypoglycaemia, hypercapnia, haemodialysis.

Question 39

What are the symptoms of idiopathic intracranial HTN?

Answer 39

Headache: Often the most common symptom, typically worse in the morning or with straining. Visual disturbances: Blurred vision, diplopia, or transient visual obscurations (brief episodes of vision loss), photopsia Pulsatile tinnitus: A whooshing sound in the ears that coincides with the heartbeat. Nausea and vomiting: May occur due to increased intracranial pressure.

Question 40

What is the diagnostic criteria for idiopathic intracranial HTN?

Answer 40

Diagnostic criteria of IIH (pseudotumor cerebri) require the presence of each of the following: A. Papilledema OR sixth (abducens) nerve palsy (unilateral or bilateral) B. Normal neurologic examination, except for papilledema and cranial nerve abnormalities C. Neuroimaging (MRI with and without gadolinium and MR venography is preferred) shows normal brain parenchyma without evidence of hydrocephalus, mass, structural lesion, or meningeal enhancement D. Normal cerebrospinal fluid (CSF) composition E. Elevated lumbar puncture opening pressure

Question 41

What is the aetiology of idiopathic intracranial HTN?

Answer 41

Idiopathic intracranial hypertension (pseudotumor cerebri): Epidemiology and pathogenesis A long list of medications have been reported to be associated with IIH. The evidence linking growth hormone treatment, retinoids, and tetracycline antibiotics is strongest; however, the mechanisms by which these might produce IIH is not known. Other than obesity, the association between other medical conditions and IIH is not proven. The pathogenesis of IIH is unknown.

Question 42

What is the treatment of idiopathic intracranial HTN?

Answer 42

Prognosis & Treatment: Refer to neuro Major complication: Vision loss (up to 25% risk of severe, permanent vision loss). Regular monitoring: Visual acuity, formal visual field tests, and dilated fundus exams. Discontinue medications like tetracycline derivatives that may worsen IIH. Treat comorbidities (e.g., sleep apnea, anemia). Recommend weight loss in obese patients for overall health benefits. Initial treatment: Acetazolamide.