Kingdom of Bahrain Arabian Gulf University College of

Kingdom of Bahrain Arabian Gulf University College of Medicine and Medical Sciences Internal Medicine Notes Neurology Prepared by: Ali Jassim Alhashli Based on: Kaplan Step 2 CK Internal Medicine

Spinal cord compression • • • Definition: back pain associated with compression of spinal cord. Etiology: – Acute: most peropably due to trauma. – Sub-acute: due to neoplasms (such as: lymphoma, multiple myeloma, prostate cancer, cancers of lung, breast, kidney or colon). – Chronic: disc herniation Clinical presentation: – Gradual onset with pain being earliest symptoms in 96% of patients. – Mild sensory disturbance (at a dermatomal sensory level). – Weakness of lower extremities (bilaterally) + upper motor neuron signs below the level of compression. – Sphincter and/or sexual dysfunction. Diagnosis: – Initial: x-ray (abnormal in 84 -94% of cases). – Diagnostic test of choice: MRI of the spine. If MRI is contraindicated → CT-myelogram is the test of choice. Treatment: – Once diagnosis is suspected: start high-dose dexamethasone (has the highest glucocorticoid activity which is needed for its anti-inflammatory effect). – After doing MRI → start your specific therapy depending on the etiology.

Spinal cord compression

Syringomyelia • • • Definition: enlargement of the spinal canal. Types: – Communicating: associated with congenital Arnold-Chiari malformation: downward displacemant and hypoplasia of cerebellum with obliteration of cisterna magna. – Non-communicating: associated with trauma or tumors of the spinal cord. Clinical manifestations: this cavitation most commonly occurs at the level of cervical cord and enlarging anteriolry resulting in: – Loss of pain and temperature sensation around the neck and arms (spinothalamic tract is affected). – Sparing sensation of light touch, vibration and position (because dorsal column is not affected). – As this cavitation progresses, it can result in LMN signs at the level of the lesion and UMN signs below the level of the lesion. Diagnosis: most accurate diagnostic test is MRI of the spine. Treatment: surgical (but unsatisfactory).

Subacute Combined Degeneration of Spinal Cord • • Occurs with: – Vitamin B 12 deficiency. – Syphilis can also cause this condition. Clinical manifestation: – Distal parasthesia (peripheral neuropathy which can also result from diabetes or alcoholism but with vitamin B 12 deficiency there is destruction of the dorsal column thus resulting also in loss of vibration and sense of position “proprioception”). Diagnosis: – ↓ serum vitamin B 12 – ↑ methymalonic acid. Treatment: replacement of vitamin B 12.

Subacute Combined Degeneration of Spinal Cord

Anterior Spinal Artery Occlusion • • Anterior spinal artery: run anterior to the spine and supplies the anterior 2/3 of the spinal cord (dorsal column is supplied by the two posterior spinal arteries and thus will not be affected in this condition). Anterior spinal artery most commonly blocked with thrombi from atrium (patient has a history of atrial fibrillation). Clinical manifestations (below the level of infarction): – Motor: flaccid paralysis evolving into spastic paresis over days to weeks. – Sensory: loss of pain and temperature with sparing of vibration and proprioception (which are carried by dorsal column). Treatment: supportive (there is nothing you can do ).

Brown-Sequard Syndrome • • Definition: hemisection of the spinal cord affecting the 3 main neural systems: – Dorsal column. – Spinothalamic tract. – Corticospinal tract. Clinical manifestations: – Ipsilateral loss of dorsal column sensations. – Ipsilateral UMN signs below the level of the lesion. – Ipsilateral LMN signs at the level of the lesion. – At the level of the lesion there is loss of all modalities of sensation (including touch, pain and temperature). – Contralateral loss of pain and temperature 12 segments below the level of the lesion.

Cerebro-Vascular Accident (Stroke) • • Definition: SUDDEN ONSET of focal neurologicdeficit. Etiology: – Ischemic: large artery thrombosis (of anterior, middle or posterior cerebral arteries); small artery thrombosis (lacunar); embolic (cardiogenic: atrial fibrillation). – Hemorrhagic: systemic hypertension; bleeding; vascular dissection (extremely rare in the brain). Risk factors (similar to those of CVD): increased age, diabetes, hypertension, hyperlipidemia and smoking. Blood supply of the brain (circle of Willis): – Carotid (anterior) circulation gives rise to: • Anterior Cerebral Arteries (ACA) which are connected anterior communicating artery. ACA supplies the medial portion of frontal and parietal lobes. • Middle Cerebral Arteries (MCA) which are supplying the lateral portions of frontal and parietal lobes in addition to the temporal lobe. – Vertebrobsilar artery (posterior circulation): • Posterior Cerebral Arteries (PCA) which are connected to the anterior circulation by posterior communicating arteries. PCA supplies portion of parietal lobe, occipital lobe, cerebellum and brainstem.

Cerebro-Vascular Accident (Stroke)

Cerebro-Vascular Accident (Stroke) • Clinical manifestations (depending on which vascular territory is affected): – Occlusion of ACA: contralateral weakness and sensory loss of lower extremity. Other common manifestations are: urinary incontinence, confusion and behavioral disturbances. – Occlusion of MCA: contralateral hemiplegia, hemisensory loss and eyes deviated toward the cortical lesion. If the lesion involves the dominant hemisphere (usually the left) → this will result in aphasia. – Occlusion of PCA: contralateral homonymous hemianopia, visual hallucinations and agnosias (inability to interpret visual information of things thus being unable to recognize them). • Posterior circulation syndromes: – Weber syndrome: ipsilateral CN III palsy with contralateral hemiplegia. – Bendikt syndrome: ipsilateral CN III palsy with contralateral ataxia. • Occlusion of major cerebellar arteries: vertigo, vomiting, nystagmus and ipsilateral limb ataxia.

Cerebro-Vascular Accident (Stroke) • • Diagnosis: – Once patient arrives to the emergency, your initial test of choice will be: non-contrast CT-scan of the head (which is more sensitive in detecting hemorrhagic stroke). – If patient is having an ischemic stoke, non-contrast CT-scan of the head will be negative within 48 hours after the onset of symptoms. – Therefore, MRI is the most accurate for detecting ischemic stoke. – If patient is having ischemic stoke, you must search for the source of emboli by doing: • ECHO. • Carotid Doppler. • Hypercoagulable studies. Treatment: – If patient presents to the emergency within 3 hours after the onset of his symptoms, TPA can be given unless contraindicated in the following conditions: • Previous stroke or head trauma within 3 months. • History of intracranial bleeding. • Bleeding (GI or genitourinary) within 3 weeks. • Surgery within 2 weeks. • Platelets < 100, 000/mm 3 – Aspirin is considered first-line treatment for secondary prevention of ischemic stoke. If there is allergy to aspirin or recurrence of cerebrovascular accident, switch the patient to clopidogrel. – In patients who have subarachnoid hemorrhage, there must be an early surgical intervention (within days) to: • Clip-off the aneurysm. • Or embolize the vessel with a catheter.

Cerebro-Vascular Accident (Stroke)

Seizures and Epilepsy • • • Definition: abnormal electrical discharge from pyramidal cells of the brain. Recurrent seizures are defined as “epilepsy”. Etiology (VITAMINS): – V: Vascular (stroke, bleeding or arteriorvenous malformation). – I: Infection (meningitis or encephalitis). – T: Trauma (especially penetrating). – A: Autoimmune (CNS vasculitis). – M: Metabolic (hypoglycemia, hyponatremia/hypernatremia, hypocalcemia that is usually associated with hypomagnesemia and hypoxia). – I: Idiopathic. – N: Neoplasms. – S: p. Sychiatric. Clinical manifestations: – Seizure is an involuntary even which has a sudden onset with or without an aura (aura: usually hallucinations which can be visual, auditory or smelling). – Patient might experience incontinence, rolling-up of his eyes and tongue biting. – After the event, patient will enter a post-ictal state during which he will be disoriented and sleepy. – It is important to differentiate between seizure and syncope when there is sudden loss of consciousness: • If patient regains consciousness rapidly: this is due to a cardiac cause. • If patient regains consciousness gradually: this is due to a neurologic cause.

Seizures and Epilepsy • Types of seizures: – Partial: in which there is a focal onset and one part of the body will be twitching. It is further classified to: • Simple partial seizure: patient is conscious. • Complex partial seizure: there is loss of consciousness. When a partial seizure progresses to generalized seizure this is known as “partial seizure with secondary generalization”. – Generalized: arising from both cerebral hemispheres. It is further classified to: • Generalized tonic-clonic (grand mal): the body becomes stiff and then jerky movements will start. • Absence seizures (petit mal): children losing their consciousness for nearly 10 seconds without loss of postural tone. It is characterized by 3 -Hz spike-andwave discharge on EEG. • Atonic seizure: sudden loss of postural tone lasting 1 -2 seconds. • Myoclonic seizure: sudden, brief muscle contraction. • Status epilepticus: recurrent or continuous seizures (lasting at least 5 -30 minutes).

Seizures and Epilepsy

Seizures and Epilepsy • • Diagnosis (you have to eliminate other causes of seizure mentioned previously) by requesting: – Head CT/MRI; serum electrolytes, blood glucose level and Arterial Blood Gas (ABG: to exclude hypoxia). – Then, ask for EEG (which is the test of choice for diagnosing epilepsy). Treatment: – Status epilepticus; • ABC: Airway (by keeping patient in left lateral position with suction of secretions); Breathing (oxygen supply); Circulation (IV fluid). • If a reversible cause is identified, treat it aggressively. • If patient continues to seize, start with benzodiazepines (lorazepam or diazepam). • If there is no improvement, add fosphenytoin. • If there is no improvement, add phenobarbital. • If still there is no improvement, intubation and anesthesia (propofol or midazolam). – When to start treatment with anticonvulsant therapy in patient presenting with first-time seizure? • Strong family history of seizure. • Patient presenting with status epilepticus. • Patient has abnormal EEG.

Seizures and Epilepsy • Anticonvulsant therapy according to the type of seizure: – Generalized tonic-clonic seizure: carbamazepine, Valproic acid is an alternative. – Absence seizures: ethosuximide. Valproic acid is an alternative. – Atonic or myoclonic seizures: valproic acid. – Partial seizures (simple or complex): carbamazepine or phenytoin. Therapy may be stopped if patient has been free of seizures for 2 -3 years.

Vertigo and Dizziness • • • Definition: vertigo = dizziness = feeling of rotation or false sensation of movement. Etiology: Central vs. peripheral – Central: it is caused by brainstem or cerebellar tumors, ischemia or hemorrhage. It has a gradual onset; absent tinnitus (buzzing in the ears) and hearing loss; presence of diplopia, extremity weakness and dysarthria; vertical nystagmus which doesn’t suppress with fixation. – Peripheral: has a sudden onset, presence of tinnitus and hearing loss; absence of diplopia, extremity weakness and dysarthria; horizontal nystagmus which suppresses with fixation. Clinical presentation: – Patient has a false sensation of movement describing it as their environment spinning around them. This is usually associated with nausea and vomiting. – You have to differentiate vertigo from pre-syncope which is characterized by: • Lightheadedness. • Generalized weakness. • Palpitations with shortness of breath. Vertigo is a manifestation of neurologic disease while presyncope is due to cardiac insufficiency.

Vertigo and Dizziness

Vertigo and Dizziness • • Differentials of peripheral vertigo: – Meniere disease: it is characterized by tinnitus, hearing loss and episodic vertigo which is lasting for 1 -8 hours depending on endolymphatic pressure as it rises and falls. Causes: head trauma and syphilis. – Benign positional vertigo: occurring when changing head position; lasting 10 -60 seconds and occurring in clusters which persist for several days. – Labyrinthitis: sudden onset of severe vertigo lasting several days with tinnitus and hearing loss; usually following an upper respiratory tract infection. – Perilymphatic fistula: occurring due to a blunt trauma to the ear, severe barotrauma during air flight, scuba diving or vigorous Valsalva maneuver. Treatment: meclizine or diazepam (in severe cases) → for symptomatic treatment – Meniere disease: low-salt diet and diuretics. – Lebyrinthitis: steroids can be used.

Headache • • Definition: headache is pain in head, jaw or neck. Etiology: – Primary headache syndromes (there is a history of recurrent symptoms): migraine, cluster and tension headaches. – Secondary causes of headache (history of first-time headache that is severe and rapidly-peaking): • Brain tumors: history of vomiting that precedes the onset of headache by a number of weeks. • Subarachenoid hemorrhage: patient will describe his headache as “the worst headache in my life”. He will have nuchal rigidity but usually no fever. • Meningitis: patient will have headache, nuchal rigidity, fever, photophobia and nausea/vomiting. • Temporal arteritis: patient’s age > 50, there is scalp tenderness (difficulty combing hair or lying on a pillow), diagnosed with biopsy of temporal artery and treated with steroids one diagnosis is suspected. • Glucoma: history of eye pain preceding the onset of headache.

Headache • • Primary headache syndromes: – Migraine headache: • Pathophysiology: vasospasm followed by vasodilation. This explains why β-blockers are used as a prophylactic treatment. • Characterized by: unilateral throbbing headache which is aggravated by minor movement, nausea and vomiting, photophobia and phonophobia. It might be accompanied by visual auras experienced as flashes of lights. • Triggers: alcohol, certain foods, hunger and irregular sleep patterns. • Treatment: – Acute episode: acetaminophen, NSAIDs or triptans (which are contraindicated in patients with cardiovascular disease, uncontrolled hypertension and pregnancy). – Prophylactic therapy (initiated when patients experiencing migraine headaches > 3 month): β-blockers (propranolol). – Tension-type headache: • Patient will experience a band-like headache bilaterally which is NOT aggravated by movement and it builds slowly. It might also be associated with tightness of posterior neck muscles. • Treatment: relaxation + acetaminophen or NSAIDs. – Cluster headache: • Commonly occurring in alcoholic males; it starts suddenly with being unilateral, periorbital and peaking within 5 minutes of onset. Attacks last 30 minutes – 3 hours and occurring 1 -3 times/day for a period of 4 -8 weeks. Associated symptoms: rhinorrhea, reddening of the eye and lacrimation. • Treatment: – Acute attack: triptans or 100% oxygen. – Prophylactic: calcium-channel blockers. Diagnosis: exclude secondary causes of headache by history and doing CT-scan of the head.

Headache

Pseudotumor Cerebri (Benign Intracranial Hypertension) • • • Definition: idiopathic increased intracranial pressure. It is a condition which is acting as if there is a brain tumor without actually having a one! Etiology: idiopathic; more common among females; might be associated with: obesity, oral contraceptives use, chronic lung disease, Addison’s disease, vitamin A toxicity and tetracycline use. Clinical presentation: – Headache. – Visual disturbances (diplopia or CN VI palsy). – Papilledema. Diagnosis: – CT/MRI of the head is normal. – CSF evaluation: showing increased intracranial pressure but otherwise it is normal. Treatment (this condition usually resolves spontaneously within several months): – Weight loss and stopping the offending agent (if present). – Diuretics (e. g. acetazolamide or furosemide). – In severe cases: repeated lumbar punctures. – If all of the above do not work: placement of surgical shunt between ventricles and peritoneum.

Trigeminal Neuralgia • • • Definition: it is an idiopathic, severe, sharp facial pain starting at the side of the mouth and progressing towards the nasal opening of the ear. Pain lasts for a few seconds. Triggers of pain: – Touch. – Facial movement (e. g. talking or eating). It is usually due to compression of trigeminal nerve by a blood vessels. Imaging and neurologic examinations are normal. Treatment: carbamazepine. If patient is not responding to medical therapy → surgery can be done (rhizotomy: cutting the nerve).

Guillain-Barre Syndrome (GBS) • • • Definition: it is an acute, autoimmune destruction of myelin sheath (demyelination will result in decreased conduction velocity). Etiology: in 75% of cases, GBS is preceded by an infection (1 -3 weeks before the onset of symptoms). Infections most commonly affecting respiratory tract or GI tract (e. g. Campylobacter jejuni). This will result in molecular mimicry and the immune system of the body will start attacking self-antigens. Clinical presentation: – Ascending paralysis: weakness more common in lower extremities and more common to distal + lack of reflexes. – Sensory disturbances: represented by pain or tingling dysthesia. – In severe cases of GBS, phrenic nerve might be affected resulting in respiratory arrest or cardiac arrhythmias. These are considered as most common causes of death in patients with GBS. Diagnosis: – Physical examination: showing the characteristic stock-and-glove pattern of weakness and loss of reflexes. – Initials test: lumbar puncture which shows increased proteins in CSF with normal cells. – Most accurate test: EMG. Treatment: – IVIG or plasmapheresis (there is no benefit to combine them). – Monitor vital capacity to prevent respiratory failure.

Guillain-Barre Syndrome (GBS)

Myasthenia Gravis (Fatigability Weakness) • • • Definition: it is a disease of neuromuscular junction in which there will be autoantibodies against Ach-receptors resulting in weakness and fatigability of muscles. Clinical presentation: – Initially: patients will present with diplopia, partial ptosis and difficulty in swallowing. – As the diseases progresses, weakness may involve proximal muscles in an asymmetric pattern. – Very severe disease may affect muscle of respiration (this is known as myesthenic crisis which can result in respiratory failure. This also occurs with cholinergic crisis in which the condition will improve when reducing the dose of cholinesterase inhibitor). Diagnosis: – Initial: Ach-receptor antibody test. – Edrophonium (Tensilon) test which is sensitive but not specific. Edrophonium will inhibit the action of Ach esterase enzyme thus increasing Ach concentration temporarily and improving patient’s symptoms. – Chest x-ray and CT to exclude presence of thymoma (in 10 -15% of patients) or thymic hyperplasia (65% of patients). – Most accurate test: EMG showing decreased muscle contraction with repetitive nerve stimulation.

Myasthenia Gravis (Fatigability Weakness)

Myasthenia Gravis (Fatigability Weakness) • Treatment: – Acute myesthenic crisis (in which there is respiratory involvement): IVIG and plasmapheresis. – Chronic management: • Start with Ach-esterase inhibitors (e. g. neostigmine or pyridostigmine). • If there is no improvement, Thymectomy. • If still there is no improvement, start immumosuppressive therapy with steroids → if patient is not responding → add azathioprine.

Amyotrophic Lateral Sclerosis (ALS) • • Definition: it is an idiopathic pure motor neuron disease with mixed manifestation of both UMN and LMN signs. Clinical manifestations: – Muscle weakness and atrophy + ↑ reflexes. Head ptosis occurs because extensor muscles of the head become weak. – Respiratory involvement: resulting in recurrent aspiration pneumonia that is considered as the most common cause of death. – Cranial nerve palsy: resulting in dysphagia, dyarthria, difficulty in chewing and absence of gag reflex. – Notice that bowel, bladder, sexual, sensory and cognitive functions are all intact. Diagnosis: EMG which shows diffuse axonal disease. Treatment: – Riluzole slowing the progression of the disease. – Spasticity is treated with baclofen. – Prognosis: death within 3 -5 (years? ? ) after diagnosis.

Amyotrophic Lateral Sclerosis (ALS)

Multiple Sclerosis (MS) • • • Definition: it is an autoimmune, inflammatory disease of CNS white matter (commonly lateral to ventricles). Etiology: idiopathic. genetic predisposition plays an important role. It is more common among females of Northern European descent and of child-bearing age. Clinical presentation: – Weakness, tingling or numbness of a limb. – Urinary urgency or retention. – Diplopia or blurred vision (Notice that and early sign of the disease could be optic neuritis: inflammation of the optic nerve). – There are mainly 3 forms of the disease: • Relapsing remitting disease: relapses of active disease with incomplete recovery during periods or remission. • Secondary progressive disease: progression becomes more aggressive. • Primary progressive disease: early onset of disability (least common form). – Suspect the diagnosis of MS when a young patient (< 55 years) presents with multiple neurologic deficits separated by time and space. – Triggers to exacerbate the disease: infection, trauma and 2 -3 months following birth (although there are fewer attacks during pregnancy).

Multiple Sclerosis (MS) • • Diagnosis: – Most accurate test: MRI of the brain. A contrast can be administered and if it is taken by the lesion this indicates that it is acute and active. – CSF analysis: • Increased WBCs (but still < 50 cells/µl). • Mildly elevated protein level. • Oligoclonal bands: recommended only when MRI is non-confirmatory but clinical suspicion of MS remains high. – Evoked response potentials are non-specific and rarely done nowadays. Treatment: – Acute exacerbation: high dose IV steroids for 3 days followed by oral steroids tapered over 4 weeks. – Disease-modifying agents: • Relapsing-remitting disease: interferon-β and glatiramer acetate. • Secondary progressive disease: interferon-β and mitoxantrone. All disease-modifying agents are relatively contraindicated in pregnancy.

Multiple Sclerosis (MS)

Dementia • • Definition: loss of memory and other cognitive functions (such as concentration, language or executive functions) interfering with patient’s daily activities. Etiology: – Reversible causes: hypothyroidism, vitamin B 12 deficiency, syphilis, hepatic/uremic encephalopathy, subdural hematoma, bleeding, CNC vasculitis, brain abscess, brain tumor, central sleep apnea, obstructive sleep apnea and depression. – Irreversible causes: • Alzheimer’s disease (accounting for 60 -80% of all dementia cases): patients presenting with memory loss followed by hallucinations and personality changes late in the course of the disease. • Dementia with Lewy bodies: Parkinson’s disease + Alzheimer’s disease. • Fronto-temporal degeneration: personality changes preceding the loss of memory. • Creutzfeldt-Jakob Disease (CJD): diagnosed by the criteria of rapidly progressing dementia (over weeks to months), myoclonus ataxia and presence of 14 -3 -3 protein in CSF. A variant of CJD is Bovine Spongiform Encephalopathy (BSE) which is transmitted through ingestion of prions from infected cattles. • Progressive Multifocal Leukoencephalopathy (PML): seen in HIV patients

Dementia • • Diagnosis: – All patient with cognitive impairment must be evaluated by Mini-Mental Status Examination (MMSE) which includes: • Orientation: time, place, person. • Memory: immediate (registration), intermediate and remote memory. • Calculation: (-7) starting from 100. • Abstract: explaining the meaning of a famous proverb. – Investigations to exclude reversible causes of dementia (mentioned previously): CBC, electrolytes, RFT, LFT, vitamin B 12, TSH/T 4, RPR/VDRL, HIV and head CT/MRI. Treatment: – Mainly aimed towards care-givers which will suffer from depression and anxiety. – Patients with Alzheimer’s disease can be given cholinesterase inhibitors (e. g. donepezil) or memantine in advanced disease.

• • Huntington Disease • • • Definition: it is an autosomal dominant degenerative disease of the brain. Etiology: presence of HD gene on chromosome 4 which contains CAG trinucleotide repeat expansion which codes for the protein huntingtin that is causing death of brain cells. Successive generations tend to have the disease occurring at an earlier age (anticipation). Clinical presentation: – Chorea: it is a neurologic disorder characterized by jerky movements affecting the face, shoulders and hips. – Personality changes: irritability, anger, paranoia and depression. – Late in the disease: dementia. Diagnosis: genetic testing for the presence of CAG trinucleotide repeat expansion. CT-scan of the head will show cerebral atrophy. Treatment: – Abnormal movements: tetrabenazine. – Personality changes: haloperidole.

Parkinson’s Disease • • • Definition: degeneration of dopaminergic neurons in substantia nigra of midbrain. Etiology: – Drugs: neuroleptic agents (e. g. haloperidol), metoclopramide, methyldopa and reserpine. – Poisoning: MPTP, carbon monoxide, cyanide and manganese. – Any structural lesion around basal ganglia. – Post-encephalitic parkinsonism. Clinical manifestations: – Bradykinesia (slow movements, mask face and reduction of autonomic movements). – Cogwheel rigidity. – Postural instability. – Resting tremor. “Parkinson plus” syndromes are those which lack response to therapy with levodopa/carbidopa (carbidopa prevents peripheral decarboxylation of levodopa thus allowing it to reach the brain). Diagnosis: clinical (it is important to exclude secondary causes of Parkinson’s disease). Treatment: – Increasing dopaminergic tone: levodopa/carbidopa. ADR: dyskinesia, restlessness and on-off phenomena. To reduce these ADR you can add a COMT inhibitor (e. g. entacapone). – Decreasing cholinergic tone (anticholinergics): benztropine. ADR: dry mouth, urinary retention, constipation and confusion/hallucinations. – If patient is < 60 years old, he has less bradykinesia and tremors are more predominant → you will start him on anticholinergic medications. When patient’s age is > 60 years with same presentation → you will start him on amantadine. – If patient is presenting mainly with significant bradykinesia → you will start him on levodopa/carbidopa. – When patient is not responding to any medical therapy → surgery is your option: • Thalamotomy (removal of subthalamic nuclei). • Deep brain stimulation of subthalamic nuclei.

Benign Essential Tremor • Definition: it is an idiopathic disorder in which the patient has isolated tremor of his hands, head or both. • Tremors are aggravated by: caffeine and β-agonists. • Tremors improve with: alcohol (2 -3 drinks) and benzodiazepines. • Treatment: – β-blockers (e. g. propranolol). – If not working, give a benzodiazepine. – If still not working, do thalamotomy.

Restless Leg Syndrome • Definition: it is an idiopathic disorder in which the patient has the sensation of creeping dysthesia in his legs resulting in involuntary movements while sleeping. • Condition is brought to attention by multiple bruises sustained by sleep partner ! • Condition is aggravated by: sleep deprivation, caffeine and pregnancy. • Treatment: dopamine agonists (e. g. pramipexole).