Management

A. Acute Treatment (Abortive)

100% Oxygen inhalation: 100% O$_2$ at 12 L/min via non-rebreather mask. Often aborts attack within 10–15 minutes.
Subcutaneous Sumatriptan: 6 mg SC $\rightarrow$ most effective. Onset within 5–10 mins. Nasal triptans less effective but may help.

Note: Oral therapies (NSAIDs, oral triptans) are too slow for cluster headaches.

B. Preventive Treatment (Prophylaxis) (Used during the cluster period)

Verapamil (first-line): 120–240 mg/day, can be increased under ECG monitoring. Most effective long-term preventive therapy.
Sodium Valproate: Useful in some patients.
Short course of Oral Steroids: Prednisolone 40–60 mg/day, tapered over 2–3 weeks. Often rapidly breaks a cluster cycle.
Lithium carbonate: Used in chronic cluster headache. Requires serum level monitoring.

Trigeminal Neuralgia (Tic Douloureux)

A condition causing recurrent, unilateral, brief, shock-like (lancinating) facial pain. Involves 2nd (maxillary) and/or 3rd (mandibular) branches of trigeminal nerve. Typically occurs in age $>50$ years. Often due to irritative compression of trigeminal root zone by an aberrant arterial loop.

Clinical Features

Pain Characteristics: Sudden, severe, stabbing, electric shock–like. Duration: seconds (very brief). Occurs in paroxysms with pain-free intervals.
Triggers: Touch, shaving, brushing teeth, cold wind, eating or talking.
Location: Unilateral, in V2 or V3 dermatomes.
Physical signs: Usually absent. Patient may sit still with facial grimace during spasms ("tic douloureux").
Course: Remitting–relapsing over years. Rare variant: Cluster–Tic syndrome (features of cluster headache + trigeminal neuralgia).

Parkinsonism

Degenerative, progressive disease affecting the basal ganglia. Syndrome consisting of a variable combination of tremor, rigidity, bradykinesia, and a characteristic disturbance of gait and posture.

Pathology

Hallmark features of PD are degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), reduced striatal dopamine, and intraneuronal proteinaceous inclusions in cell bodies and axons that stain for $\alpha$-synuclein (known as Lewy bodies and Lewy neurites; collectively as Lewy pathology).

Clinical Features

A. Motor Features

Tremor: Resting, 3–4 Hz, “pill-rolling.” Asymmetric onset. Affects limbs, jaw, chin; never head.
Bradykinesia: Fundamental feature. Slowness, reduced amplitude, fatigability. Micrographia. Difficulty initiating movement (gait ignition failure).
Rigidity: Cogwheel rigidity (due to tremor + rigidity). Lead-pipe rigidity.
Postural & Gait Abnormalities: Stooped posture. Loss of postural reflexes $\rightarrow$ falls. Festinant gait (short, rapid steps). Freezing in doorways.

B. Non-Motor Features

Cognitive impairment, dementia.
Anxiety, depression, apathy.
Hallucinations/psychosis.
Sleep disturbance & hypersomnolence.
Constipation, sexual dysfunction, drooling, weight loss.
Autonomic symptoms.

Investigations

Diagnosis is clinical.
A. Imaging: CT/MRI usually normal for age $\rightarrow$ rarely helpful. Used only to support suspected alternative causes (e.g., vascular parkinsonism).
B. Functional imaging: SPECT/PET shows reduced dopaminergic activity early. Does not differentiate PD from atypical degenerative parkinsonis