Neurological Disorders Cheatsheet

Cheatsheet Content

Pyogenic (Bacterial) Meningitis – Internal Medicine Focus (In-Depth) Definition & Epidemiology (Davidson's p. 1106) Definition: Acute inflammation of the meninges caused by bacterial infection, primarily affecting the subarachnoid space. Characterized by purulent exudate. A medical emergency with high morbidity and mortality if not treated promptly. Incidence: ~1-3 cases per 100,000 population per year in developed countries. Mortality: 5-10% in adults, higher in elderly, immunocompromised, and with delayed presentation/treatment. Survivors often suffer neurological sequelae: hearing loss (most common), cognitive impairment, focal neurological deficits, hydrocephalus, seizures. Etiology (Common Pathogens) (Davidson's p. 1106) Pathogens vary significantly with age and predisposing factors: Neonates ($\leq 1$ month): Group B Streptococcus (GBS), E. coli, Listeria monocytogenes. Infants/Children (1 month - 5 years): Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b (Hib - incidence greatly reduced by vaccination). Children/Adolescents (5-29 years): Neisseria meningitidis, Streptococcus pneumoniae. Adults (30-59 years): Streptococcus pneumoniae, Neisseria meningitidis. Elderly ($\geq 60$ years): Streptococcus pneumoniae, Listeria monocytogenes, Gram-negative bacilli (e.g., Klebsiella, E. coli). Specific Risk Factors: Immunocompromised (e.g., HIV, organ transplant, chemotherapy, chronic alcoholism): Listeria, Gram-negative bacilli, S. pneumoniae, N. meningitidis. Post-neurosurgery/Head Trauma (especially with CSF leak or shunt): Staphylococcus aureus (including MRSA), Coagulase-negative Staphylococci, Gram-negative bacilli (e.g., Pseudomonas aeruginosa). Splenectomy: Encapsulated organisms (S. pneumoniae, N. meningitidis, H. influenzae). Pathophysiology (Davidson's p. 1106) Colonization: Pathogens (e.g., S. pneumoniae, N. meningitidis) colonize the nasopharynx. Invasion: Bacteria invade the bloodstream, leading to bacteremia. Breach of Blood-Brain Barrier (BBB): Bacteria cross the BBB, often via the choroid plexus or cerebral microvasculature, gaining access to the subarachnoid space. Inflammation: In the subarachnoid space, bacteria multiply rapidly due to limited host defenses. Bacterial components (e.g., LPS, teichoic acid) trigger a massive inflammatory response. Consequences of Inflammation: Increased BBB permeability $\rightarrow$ vasogenic cerebral edema. Leukocyte migration into CSF and release of cytotoxic mediators $\rightarrow$ cytotoxic cerebral edema. Increased intracranial pressure (ICP) due to edema and impaired CSF outflow. Inflammation of cerebral blood vessels (vasculitis), leading to thrombosis and reduced cerebral blood flow $\rightarrow$ ischemic damage (infarcts). Neuronal damage from direct bacterial toxins, excitotoxicity, and apoptosis. Clinical Presentation (Davidson's p. 1106) Classic Triad (present in ~44% of adults): Fever ($\geq 38^{\circ}$C) Headache (severe, diffuse, often frontal or retro-orbital) Nuchal Rigidity (stiff neck) Other Common Symptoms & Signs: Altered mental status (confusion, lethargy, irritability, stupor, coma) – present in $>75\%$ of cases. Photophobia, phonophobia. Nausea and vomiting. Seizures (15-30% of cases). Focal neurological deficits (e.g., cranial nerve palsies [III, IV, VI, VII, VIII], hemiparesis, dysphasia) – indicate complications. Papilledema (swelling of optic disc) – suggests increased ICP, usually a late sign. Meningeal Signs (less reliable in very young, very old, or severely obtunded patients): Nuchal Rigidity: Inability to passively flex the neck forward due to spasm of neck extensors. Kernig's Sign: Inability to fully extend the leg passively when the hip is flexed 90 degrees. Brudzinski's Sign: Passive flexion of the neck causes involuntary flexion of the hips and knees. Specific to Neisseria meningitidis: Petechial or purpuric rash (non-blanching), rapidly progressive septic shock (Waterhouse-Friderichsen syndrome). Diagnosis (Davidson's p. 1107) Prompt diagnosis is crucial. Investigations should not delay empiric treatment. Initial Steps Clinical Suspicion. Blood Cultures: Always draw cultures (at least two sets) BEFORE antibiotics if possible. CT Head Scan (Non-contrast): Perform BEFORE lumbar puncture (LP) if any of the following are present (to rule out mass effect/herniation risk): Immunocompromised state. History of CNS disease (e.g., mass lesion, stroke). New onset seizure within 1 week of presentation. Papilledema. Abnormal level of consciousness (GCS Focal neurological deficit. If CT is abnormal or LP is delayed, administer empiric antibiotics immediately after blood cultures. Lumbar Puncture (LP): Essential for definitive diagnosis. Obtain CSF for analysis. CSF Analysis (Davidson's p. 1107) Parameter Normal Pyogenic Meningitis Appearance Clear, colorless Turbid/Cloudy Opening Pressure (cm H2O) 5-20 Elevated (>25-30) White Blood Cells (cells/$\mu$L) Elevated (1000-5000, can be >10,000) Predominant Cell Type Mononuclear Neutrophils (>80%, often >90%) Protein (mg/dL) Markedly Elevated (>100-500, can be >1000) Glucose (mg/dL) 50-80 (or >60% plasma glucose) Low ( CSF:Blood Glucose Ratio >0.6 Gram Stain Negative Positive (60-90% sensitivity) Culture Sterile Positive (70-85% sensitivity) Other CSF Tests: Latex Agglutination Tests, PCR for specific bacterial pathogens, CSF lactate >3.5 mmol/L (differentiates from viral). Management (Davidson's p. 1107-1108) Bacterial Meningitis – Initiate Empiric Antibiotics STAT! Empiric Antibiotic Regimen (IV): Based on age and risk factors. Administer immediately after blood cultures and LP (or CT if LP delayed). Adults Ceftriaxone (2 g q12h) or Cefotaxime (2 g q4-6h) + Vancomycin (15-20 mg/kg q8-12h). Adults $\geq 60$ years OR Immunocompromised: Ceftriaxone/Cefotaxime + Vancomycin + Ampicillin (2 g q4h) (for Listeria coverage). Post-neurosurgery/Head Trauma/Shunt Infection: Vancomycin + Cefepime (2 g q8h) or Meropenem (1 g q8h). Penicillin Allergic: Moxifloxacin (400 mg daily) + Vancomycin. If severe allergy, Meropenem + Vancomycin. Dexamethasone (IV): 0.15 mg/kg IV q6h for 2-4 days. Initial dose given 15-20 minutes BEFORE or concurrently with the first dose of antibiotics. Reduces inflammation and neurological complications, especially in S. pneumoniae meningitis. Discontinue if non-S. pneumoniae bacterial meningitis is confirmed or if aseptic meningitis. Supportive Care: Monitor vital signs, neurological status, ICP. Fluid management, antipyretics, anticonvulsants. Treat complications (e.g., hydrocephalus, SIADH). Targeted Therapy: Adjust antibiotics once culture and susceptibility results are available. Duration typically 7-21 days depending on pathogen. N. meningitidis: Penicillin G or Ceftriaxone (7 days). S. pneumoniae: Penicillin G, Ceftriaxone, or Vancomycin (if resistant) (10-14 days). Listeria monocytogenes: Ampicillin (21 days). Prognosis & Complications (Davidson's p. 1108) Mortality: 5-10% in adults. Predictors of poor outcome: advanced age, delayed treatment, low GCS, seizures, specific pathogens (e.g., S. pneumoniae). Neurological Sequelae: Hearing loss (most common), cognitive impairment, focal neurological deficits (e.g., cranial nerve palsies), hydrocephalus, seizures. Prevention (Davidson's p. 1108) Vaccination: Pneumococcal, Meningococcal, Hib vaccines. Chemoprophylaxis: For close contacts of N. meningitidis (Rifampicin, Ciprofloxacin, or Ceftriaxone) or H. influenzae type b (Rifampicin). Tuberculous Meningitis (TBM) – Internal Medicine Focus (In-Depth) Definition & Epidemiology (Davidson's p. 1107) Definition: Inflammation of the meninges caused by Mycobacterium tuberculosis. Most severe form of extrapulmonary tuberculosis. More common in developing countries, but rising in developed countries due to immigration and HIV co-infection. High mortality and neurological morbidity even with treatment. Pathophysiology (Davidson's p. 1107) Occurs due to hematogenous spread of M. tuberculosis from a primary focus (often lungs) to the subarachnoid space, forming small subpial or subependymal foci called Rich foci. Rupture of these Rich foci into the subarachnoid space triggers an intense inflammatory response. Characteristic pathology: Thick gelatinous exudate in the basal cisterns, leading to: Hydrocephalus (communicating or obstructive) due to blockage of CSF flow. Cranial nerve palsies (especially III, VI, VII) due to entrapment in the exudate. Vasculitis (tuberculous arteritis) of cerebral blood vessels, leading to ischemic infarcts. Tuberculomas (intracranial granulomas). Clinical Presentation (Davidson's p. 1107) Typically subacute onset, evolving over 2-8 weeks, unlike acute pyogenic meningitis. Prodromal symptoms: Low-grade fever, malaise, anorexia, headache. Stage I: Non-specific symptoms, mild headache, lethargy, irritability. No neurological deficits. Stage II: Meningeal signs (nuchal rigidity), cranial nerve palsies, focal neurological deficits, seizures, altered mental status. Stage III: Stupor, coma, severe neurological deficits, decorticate/decerebrate posturing, hydrocephalus. Evidence of extrapulmonary TB (e.g., lymphadenopathy, pulmonary infiltrates) may or may not be present. Diagnosis (Davidson's p. 1107) Diagnosis requires high clinical suspicion and CSF analysis. CSF Analysis Parameter Tuberculous Meningitis Appearance Clear or xanthochromic Opening Pressure (cm H2O) Elevated White Blood Cells (cells/$\mu$L) Elevated (100-500) Predominant Cell Type Lymphocytes/Mononuclear (>50%, early may be neutrophilic) Protein (mg/dL) Markedly Elevated (100-500, can be >1000) Glucose (mg/dL) Low ( CSF:Blood Glucose Ratio Gram Stain Negative Culture Positive (slow, can take weeks) Specific CSF Tests: Acid-fast bacilli (AFB) stain (low sensitivity), mycobacterial culture (gold standard, slow), CSF PCR for M. tuberculosis (higher sensitivity), CSF Adenosine Deaminase (ADA). Neuroimaging (MRI with contrast): Essential. May show basal meningeal enhancement, hydrocephalus, tuberculomas, or infarcts. Other investigations: Chest X-ray, tuberculin skin test (TST) or interferon-gamma release assay (IGRA). Management (Davidson's p. 1107) Treatment should be initiated promptly on suspicion, even before microbiological confirmation. Anti-tuberculous Therapy: Prolonged multi-drug regimen, typically for 9-12 months. Initial intensive phase (2 months): Isoniazid (H), Rifampicin (R), Pyrazinamide (Z), Ethambutol (E) (RIPE regimen). Continuation phase (7-10 months): Isoniazid and Rifampicin. Dosages need to be adjusted for CNS penetration. Corticosteroids (Dexamethasone): Essential for reducing mortality and neurological complications. Started concurrently with antituberculous drugs and tapered slowly over 6-8 weeks. Management of Complications: Hydrocephalus (may require CSF shunt), increased ICP, seizures. Peripheral Neuropathy – Internal Medicine Focus (In-Depth) Definition & Classification (Davidson's p. 1131-1132) Definition: Damage to nerves outside the brain and spinal cord (peripheral nervous system). Can affect motor, sensory, and autonomic nerves. Classification by Anatomy: Mononeuropathy: Damage to a single peripheral nerve (e.g., carpal tunnel syndrome - median nerve). Mononeuropathy Multiplex: Damage to multiple, distinct peripheral nerves (e.g., vasculitic neuropathy). Polyneuropathy: Symmetrical, generalized damage to many peripheral nerves (most common type, e.g., diabetic neuropathy). Plexopathy: Damage to a nerve plexus (e.g., brachial or lumbosacral plexus). Radiculopathy: Damage to nerve roots (e.g., due to disc herniation). Classification by Pathophysiology: Axonal Neuropathy: Damage to the nerve axon. Leads to Wallerian degeneration. Characterized by reduced amplitude of nerve action potentials. Demyelinating Neuropathy: Damage to the myelin sheath around the axon. Slows nerve conduction. Characterized by reduced nerve conduction velocity and/or conduction block. Mixed axonal and demyelinating features can occur. Etiology (Common Causes of Polyneuropathy) (Davidson's p. 1132-1133) Metabolic/Endocrine: Diabetes Mellitus (most common cause): Distal symmetrical polyneuropathy, autonomic neuropathy, mononeuropathies. Uremia (chronic kidney disease). Hypothyroidism. Vitamin deficiencies (B1, B6, B12, E, folate). Inflammatory/Autoimmune: Guillain-Barré Syndrome (GBS): Acute demyelinating polyneuropathy (AIDP). Rapidly progressive, ascending paralysis. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): Chronic, relapsing or progressive demyelinating neuropathy. Vasculitic neuropathy (e.g., polyarteritis nodosa, granulomatosis with polyangiitis). Connective tissue diseases (e.g., SLE, Sjögren's syndrome, rheumatoid arthritis). Paraproteinemia (e.g., multiple myeloma, MGUS). Toxic: Alcohol: Alcoholic neuropathy (often due to associated nutritional deficiencies). Heavy metals (lead, arsenic, mercury). Drugs (e.g., chemotherapy - vincristine, cisplatin, taxanes; isoniazid, amiodarone, phenytoin, metronidazole). Infectious: HIV/AIDS. Lyme disease. Diphtheria. Leprosy. Herpes Zoster (post-herpetic neuralgia). Genetic/Inherited: Charcot-Marie-Tooth disease (CMT) - heterogeneous group of inherited neuropathies. Hereditary amyloidosis. Other: Critical illness polyneuropathy/myopathy. Malignancy (paraneoplastic syndromes). Idiopathic (cryptogenic) - up to 20% of cases. Clinical Presentation (Davidson's p. 1132) Symptoms depend on the type of nerve fibers affected (sensory, motor, autonomic) and the distribution. Sensory Symptoms (most common): Positive symptoms: Paresthesias (tingling, pins and needles), dysesthesias (unpleasant abnormal sensations), burning pain, shooting pain, allodynia (pain from non-painful stimuli). Negative symptoms: Numbness, loss of vibration sense, proprioception, light touch, temperature. Distribution: Often "glove and stocking" distribution in polyneuropathy, starting distally. Motor Symptoms: Weakness (distal > proximal often). Muscle cramps, fasciculations. Difficulty with fine motor tasks (e.g., buttoning). Foot drop, gait disturbance. Muscle atrophy (late sign). Autonomic Symptoms: Orthostatic hypotension (dizziness on standing). Gastroparesis (nausea, early satiety, vomiting). Bladder dysfunction (urinary retention/incontinence). Erectile dysfunction. Sweating abnormalities, dry eyes/mouth. Examination Findings: Reduced/absent ankle jerks (early sign of polyneuropathy). Reduced vibration and proprioception (often early). Distal weakness, foot drop. Trophic changes (skin dryness, hair loss, nail changes). Diagnosis (Davidson's p. 1133) A detailed history and neurological examination are crucial to characterize the neuropathy (type, distribution, onset, progression). Electrodiagnostic Studies (EMG & NCS): Nerve Conduction Studies (NCS): Measure nerve conduction velocity, amplitude, and latency. Differentiates axonal from demyelinating neuropathy. Electromyography (EMG): Assesses muscle electrical activity. Identifies denervation (fibrillations, positive sharp waves) and reinnervation (large motor unit potentials). Helps localize lesions (root, plexus, nerve). Laboratory Tests (to identify underlying cause): Fasting glucose, HbA1c (for diabetes). Renal and liver function tests. Thyroid function tests. Vitamin B12, folate levels. ESR, CRP, ANA, anti-dsDNA, ENA (for autoimmune/inflammatory). Serum and urine protein electrophoresis with immunofixation (for paraproteinemia). HIV serology, Lyme serology. Heavy metal screen (if suspected). Genetic testing (if inherited neuropathy suspected, e.g., CMT). Other Tests: Nerve Biopsy: Rarely performed, but can be helpful in specific cases (e.g., vasculitis, amyloidosis). Autonomic Function Testing: For suspected autonomic neuropathy. Skin Biopsy (for small fiber neuropathy): Measures intraepidermal nerve fiber density. Management (Davidson's p. 1133-1134) Treatment focuses on managing the underlying cause and symptomatic relief. Treating the Underlying Cause: Diabetes: Strict glycemic control. Vitamin Deficiencies: Supplementation (e.g., B12 injections). Autoimmune/Inflammatory: Immunosuppression (corticosteroids, IVIG, plasma exchange, other immunomodulators) for GBS, CIDP, vasculitis. Toxic Neuropathy: Remove offending agent (e.g., stop alcohol, chelation for heavy metals). Uremia: Dialiasis or kidney transplant. Symptomatic Management (for neuropathic pain): First-line: Gabapentin (start 300 mg QHS, titrate up to 1800-3600 mg/day in divided doses). Pregabalin (start 75 mg BID, titrate up to 300-600 mg/day in divided doses). Duloxetine (SNRI, 30-60 mg daily). Amitriptyline (TCA, start 10-25 mg QHS, titrate up to 75-150 mg QHS). Topical agents: Capsaicin cream, lidocaine patches. Physical therapy: For weakness, gait instability. Orthotics/Splints: For foot drop. Patient Education: Foot care (especially in diabetes), fall prevention, regular exercise. Clinical Localization of Spinal Cord Lesions General Principles of Localization Spinal cord lesions are localized by identifying the highest level of abnormality based on dermatomal sensory loss, myotomal motor weakness, and reflex changes. Distinguish between spinal cord level (segment of the cord) and vertebral level (bone level). The spinal cord is shorter than the vertebral column, so cord segments are higher than their corresponding vertebral bodies, especially in the lumbar region. Sensory Level: The highest dermatome with altered sensation. This is often the most reliable sign. Motor Level: The lowest myotome with normal strength. Reflex Changes: Hyporeflexia/Areflexia: Suggests a lower motor neuron (LMN) lesion at or below the level of the reflex arc. Hyperreflexia: Suggests an upper motor neuron (UMN) lesion above the reflex arc. Bowel/Bladder Dysfunction: Often indicates sacral (S2-S4) involvement. Autonomic Dysfunction: Orthostatic hypotension, impaired sweating. Key Spinal Cord Levels for Localization Spinal Cord Segment Motor Examination Sensory Examination Reflexes C5 Deltoid (shoulder abduction), Biceps (elbow flexion) Lateral arm (over deltoid) Biceps reflex (C5/C6) C6 Wrist extensors, Biceps Thumb, lateral forearm Brachioradialis reflex (C5/C6) C7 Triceps (elbow extension), Wrist flexors, Finger extensors Middle finger Triceps reflex (C7/C8) C8 Finger flexors Little finger, medial forearm T1 Finger abductors Medial arm T4 Nipple line T10 Umbilicus L2 Hip flexion (Psoas) Anterior thigh L3 Knee extension (Quadriceps) Medial thigh/knee L4 Ankle dorsiflexion (Tibialis anterior) Medial leg, medial malleolus Patellar reflex (L3/L4) L5 Great toe dorsiflexion (Extensor hallucis longus) Dorsum of foot, lateral leg S1 Ankle plantarflexion (Gastrocnemius) Lateral foot, sole Achilles reflex (S1/S2) S2-S4 Anal sphincter tone Perianal sensation Bulbocavernosus reflex, Anal wink Patterns of Spinal Cord Syndromes (to aid localization) Complete Transverse Myelopathy: Bilateral loss of all sensory modalities, motor function, and autonomic function below the lesion. UMN signs below, LMN signs at the lesion level. Brown-Séquard Syndrome (Hemisection): Ipsilateral: Loss of proprioception, vibration, and motor function below the lesion (UMN). LMN signs at the lesion level. Contralateral: Loss of pain and temperature sensation below the lesion (typically 1-2 segments below the lesion due to crossing of spinothalamic tracts). Central Cord Syndrome (often cervical): Affects central gray matter. Disproportionately greater motor weakness in upper extremities than lower extremities. "Cape-like" or "suspended" sensory loss (pain/temperature) due to involvement of crossing spinothalamic fibers. Preservation of proprioception and vibration (dorsal columns spared). Anterior Cord Syndrome: Affects anterior 2/3 of cord (motor tracts, spinothalamic tracts). Bilateral paralysis and loss of pain/temperature sensation below the lesion. Preservation of proprioception and vibration (dorsal columns spared). Posterior Cord Syndrome: Affects dorsal columns. Bilateral loss of proprioception and vibration below the lesion. Preservation of motor function, pain, and temperature sensation. Clinical Features of Intramedullary Lesion at C4-C6 An intramedullary lesion arises within the spinal cord parenchyma itself (e.g., syringomyelia, tumor, central disc herniation, demyelinating plaque). A lesion at the C4-C6 cervical level often presents with a combination of UMN and LMN signs, and a characteristic sensory pattern, typically consistent with a Central Cord Syndrome due to the central location of the lesion affecting crossing fibers and medial motor tracts. Key Clinical Features at C4-C6 Level Motor Dysfunction: Upper Extremity Weakness: LMN signs (at level C4-C6): Weakness, atrophy, and fasciculations in muscles innervated by C4, C5, and C6 segments (e.g., deltoids, biceps, brachioradialis, wrist extensors). This is due to direct damage to anterior horn cells. UMN signs (below level C4-C6): Spasticity, hyperreflexia, and Babinski sign in muscles innervated below C6 (e.g., triceps, hand intrinsics, and all lower extremity muscles). This is due to damage to descending corticospinal tracts. Disproportionate weakness: Typically, upper extremity weakness is more pronounced than lower extremity weakness, a hallmark of central cord syndrome. Lower Extremity Weakness: Generally UMN type (spasticity, hyperreflexia, Babinski), but may be less severe than upper extremity weakness due to the more medial location of lower extremity tracts in the corticospinal pathway. Sensory Dysfunction: "Cape-like" or "Suspended" Sensory Loss: Loss of pain and temperature sensation in a distribution corresponding to the C4-C6 dermatomes (e.g., over the shoulders, upper arms, lateral forearms, and thumbs). This occurs due to damage to the crossing spinothalamic fibers in the central gray matter. Preservation of Dorsal Column Senses: Proprioception, vibration, and light touch are often preserved, as the dorsal columns (carrying these sensations) are located more peripherally in the white matter and are typically spared by central intramedullary lesions. Sensory deficits below C6 (i.e., trunk and legs) may be less affected or spared, or show a less severe and often dissociated loss of pain/temperature. Reflex Changes: Hyporeflexia/Areflexia (at level): Reduced or absent biceps (C5/C6) and brachioradialis (C5/C6) reflexes due to LMN involvement. Hyperreflexia (below level): Exaggerated triceps (C7/C8) and lower extremity reflexes (patellar, Achilles) due to UMN involvement. Autonomic Dysfunction: May include bladder dysfunction (urgency, retention), bowel dysfunction, and sexual dysfunction. Horner's syndrome (ptosis, miosis, anhidrosis) can occur if the intermediolateral cell column (sympathetic outflow) at T1 is also affected, or if there is ascending sympathetic fiber damage from lower cervical regions. Pain: Localized neck pain, radicular pain into the arms, or neuropathic burning pain. Specific Considerations for Intramedullary Lesions Syringomyelia: A common cause of central cord syndrome. Characterized by a fluid-filled cavity (syrinx) within the spinal cord. Typically causes progressive "cape-like" sensory loss and LMN weakness at the level of the syrinx, with later UMN signs below. Intramedullary Tumors: Can cause similar symptoms, often with a more progressive course. Early vs. Late Presentation: Early lesions may present with more subtle or isolated symptoms. As the lesion expands, it affects more tracts, leading to a more complete central cord syndrome. Asterixis and Involuntary Movement Disorders Asterixis ("Flapping Tremor") Definition: A sudden, brief, involuntary jerking movement, often described as a "flapping" tremor, especially of the outstretched hands. It results from a brief, transient loss of muscle tone. Mechanism: Thought to be due to an intermittent disruption of afferent input to the motor cortex or cerebellar outflow, leading to a temporary failure of sustained muscle contraction. Not a true tremor. Elicitation: Ask the patient to extend their arms, dorsiflex their wrists, and spread their fingers. Observe for irregular, brief, flapping movements. Can also be observed in other body parts (e.g., feet, tongue, eyelids). Causes (Metabolic Encephalopathies are primary): Hepatic Encephalopathy (most common): Due to liver failure. Uremic Encephalopathy: Due to kidney failure. Hypercapnic Encephalopathy: Due to severe respiratory failure (e.g., COPD exacerbation). Hypoglycemia. Hypomagnesemia, Hypokalemia. Drug Intoxication: Barbiturates, benzodiazepines, antiepileptic drugs. Wilson's Disease: A genetic disorder of copper metabolism. Clinical Significance: A key clinical sign of metabolic encephalopathy, indicating severe systemic dysfunction affecting brain function. Involuntary Movement Disorders (Dyskinesias) A broad category of neurological disorders characterized by unwanted, uncontrolled movements. Often involve the basal ganglia circuits. 1. Tremor Definition: Rhythmic, oscillatory movement of a body part. Classification: Resting Tremor: Occurs at rest, diminishes with voluntary movement (e.g., Parkinson's disease - "pill-rolling" tremor, 4-6 Hz). Action Tremor: Occurs during voluntary movement. Postural Tremor: Occurs while maintaining a posture (e.g., holding arms outstretched). Common in Essential Tremor (6-12 Hz, often bilateral, symmetrical, affecting hands, head, voice). Also seen in anxiety, hyperthyroidism, drugs. Kinetic/Intention Tremor: Occurs during movement, worsens as target is approached (e.g., cerebellar disease, multiple sclerosis). Investigation: Clinical observation, accelerometry, EMG. Treatment: Beta-blockers (propranolol) for essential tremor, primidone. Levodopa for Parkinsonian tremor. Deep Brain Stimulation (DBS) for refractory cases. 2. Dystonia Definition: Sustained or intermittent muscle contractions causing abnormal, often repetitive, movements and/or postures (e.g., twisting, repetitive movements, or abnormal fixed postures). Types: Focal Dystonia: Affects a single body part (e.g., cervical dystonia/spasmodic torticollis, blepharospasm, writer's cramp). Segmental Dystonia: Affects contiguous body parts. Generalized Dystonia: Affects trunk and at least two other body parts. Causes: Primary (genetic), secondary (e.g., drugs like neuroleptics, stroke, trauma, Wilson's disease). Tardive dystonia from chronic dopamine blockers. Treatment: Botulinum toxin injections for focal dystonias, oral medications (anticholinergics, benzodiazepines, baclofen), DBS for generalized dystonias. 3. Chorea Definition: Irregular, unpredictable, brief, jerky, non-stereotyped movements that flow from one body part to another. Appears dance-like. Causes: Huntington's Disease: Genetic neurodegenerative disorder. Sydenham's Chorea: Post-streptococcal, associated with rheumatic fever. Drug-induced: Levodopa, neuroleptics (tardive dyskinesia), oral contraceptives. Metabolic: Hyperthyroidism, hyperglycemia. Autoimmune: SLE. Treatment: Dopamine antagonists (tetrabenazine, valbenazine, deutetrabenazine). 4. Athetosis Definition: Slow, writhing, involuntary movements, especially of the distal extremities. Often blends into dystonia. Causes: Often associated with cerebral palsy, basal ganglia lesions. 5. Hemiballismus Definition: Large amplitude, wild, flinging, involuntary movements of one side of the body, usually involving proximal musculature. Causes: Typically due to a lesion in the contralateral subthalamic nucleus (e.g., stroke, hemorrhage). Treatment: Dopamine blocking agents. 6. Myoclonus Definition: Sudden, brief, shock-like involuntary jerks caused by muscle contractions (positive myoclonus) or inhibitions (negative myoclonus, e.g., asterixis). Types: Physiological (e.g., hypnic jerks), essential, epileptic, symptomatic (e.g., metabolic, anoxic brain injury, neurodegenerative diseases). Treatment: Clonazepam, valproate, levetiracetam. 7. Tics Definition: Sudden, rapid, recurrent, non-rhythmic motor movements or vocalizations. Can be suppressible. Types: Motor Tics: Simple (e.g., eye blinking, head jerking), complex (e.g., touching, jumping). Vocal Tics: Simple (e.g., throat clearing, grunting), complex (e.g., coprolalia, echolalia). Causes: Tourette's syndrome (multiple motor tics and at least one vocal tic), chronic tic disorder, transient tic disorder. Treatment: Behavioral therapy (CBIT), alpha-2 agonists (guanfacine, clonidine), dopamine blockers (aripiprazole, haloperidol, risperidone).