neuro, psych, opthalmo Flashcards

Question

Weber's syndrome,

Answer 1

3rd nerve palsy with contralateral hemiplegia characterized by damage to the midbrain, resulting in an ipsilateral (same side) oculomotor nerve palsy and a contralateral (opposite side) hemiplegia (paralysis or weakness).

Answer 2

disorder of eye movement caused by damage to the medial longitudinal fasciculus (MLF) causes - MS, Stroke on the side that failed to adduct has the leision

Answer 3

fatal neurological disease caused by the JC virus, JC virus is activated by Nataluzumab- MS, weakened immune systems, HIV, transplantation

Answer 4

a sudden increase in floaters (small dark spots or shapes) and flashes of light, which can be brief streaks in the peripheral vision

Answer 5

IV cephalosporin and metronidazole

Answer 6

genetic, progressive muscle-weakening condition primarily affecting the face, shoulders, and upper arms, but can spread to other muscles. It is inherited in an autosomal dominant pattern,

Answer 7

dopamine agonists - ropinirole, pramipexole and rotigotine, connected with periodic limb movement disorder

Answer 8

pervasive and long-standing pattern of distrust and suspicion of others, leading to difficulties in forming and maintaining relationships, overly sensitive

Answer 9

disruption of the sympathetic nerve pathway supplying the head and neck, leading to characteristic symptoms like miosis (constricted pupil), ptosis (drooping eyelid), and anhidrosis (decreased sweating) on the affected side The Sympathetic Nerve Pathway present as - Miosis, Ptosis, Anhidrosis, Enophthalmos, Anisocoria causes -Central lesions,

Answer 10

surgical - pupils dont respond to light due to external compression from anurism, false localizing sign- unckle hereniation medical - spares the pupils, diabetes, athlesclerosis

Answer 11

Common in age-related macular degeneration (AMD) visual hallucinations in people with sight loss Risk Factors - Eye Conditions Leading to Low Vision, Advanced Age, Bilateral Vision Loss, Psychological Factors, reassure them

Answer 12

**D**istal weakness, autosomal **d**ominent, **d**istruption in the hormonal, **d**isathriya, **d**iabetes, **d**ispagia, learning diffiulty

Answer 13

seizure that happens while a person is awake and alert and aware of what is going on

Answer 14

caused by trauma, stroke, tumors

Answer 15

parietal - inferer temporal - superior

Answer 16

leisions before the Chiasm - affects one eye - anopia post chiasmal leisons - hormonemous defects congruous - optic radiation, oxypital cortex more posterer the defect more congruous defects incongrous - optic tract leisons (IT)

Answer 17

cause tremor, confusion, auditory and v halucinatins, fever, tachicardia

Answer 18

Triad - gait disturbance, cognitive impairment, and urinary incontinence

Answer 19

a neurological disorder caused by a stroke in the lateral part of the medulla oblongata, often due to a blockage in the vertebral or PICA arteries ataxia, same side facial numbness, horners sysndrome (ptosis, miosys, anhydrosis) contralateral pain & temp loss

Answer 20

Quatiapine

Answer 21

Dopamine D2 receptor antagonist

Answer 22

fever, muscle regidity , autonomic lability, hyertension, tachicardia, tachypnea, dopamine blockade treatment - dandrolin, iv fluid, bromocriptine dopamine agonist

Answer 23

acute - triptan(contraindicated in CVS Disease) + NSAID/ paracetamol Opioids contraindicated

Answer 24

ondansetron, granisetron, dolasetron, and palonosetron side effect - constipation common

Answer 25

Mamilary body enhancement due to petacheal haemorrage

Answer 26

levadopa - motor symptoms

Answer 27

confusion ataxia nistagmus opthalmoplegia pheripheral neurpathy CAN OPEN ✅ Always give thiamine BEFORE glucose in at-risk patients. ✅ MRI is not required for diagnosis – treat empirically if clinical suspicion is high. ✅ Korsakoff psychosis is preventable with timely thiamine. Diagnosis 1. Clinical Suspicion (High mortality if untreated!). 2. Labs: Thiamine levels (low, but often unavailable urgently). MRI Brain: T2/FLAIR hyperintensities in mammillary bodies, thalamus, periaqueductal gray matter. Note: MRI may be normal in early stages. 3. Response to Thiamine: Improvement supports diagnosis. Management (Urgent!) 1. Thiamine Replacement: IV/IM Thiamine (500 mg 3× daily for 2–3 days) → then 250 mg daily for 3–5 days or until no further improvement. Oral thiamine (100 mg daily) for chronic deficiency. Give before glucose (to prevent worsening symptoms). 2. Supportive Care: Correct electrolyte imbalances (Mg²⁺, K⁺). Monitor for Korsakoff’s psychosis (chronic memory disorder). Complications Korsakoff’s Psychosis (irreversible anterograde amnesia, confabulation). Death (untreated cases: 20% mortality). Key Takeaways ✅ Suspect in alcoholism/malnutrition + confusion/ataxia/eye signs. ✅ IV thiamine immediately – do not wait for lab/MRI confirmation. ✅ MRI findings: Mammillary bodies/thalamic lesions.

Answer 28

unable form new momories recover within hours no increase risk of stroke

Answer 29

if liver cirosis present - loreziopam chlordiazepoxide - p450, hepatic oxidtion, can cause drug accumilation and toxicity# A life-threatening complication of alcohol withdrawal characterized by autonomic hyperactivity, severe confusion, and hallucinations. Key Features Onset: 48–96 hours after last drink (peaks at 72 hours). Duration: 3–5 days (can be fatal if untreated). Hallmark Triad: Altered mental status (delirium, agitation). Autonomic instability (tachycardia, hypertension, fever). Gross tremor ("the shakes"). Symptom Details Neurologic Confusion, hallucinations (visual > auditory), seizures. Autonomic Tachycardia (>120), hypertension, sweating, fever. Psychiatric Severe anxiety, paranoia, agitation. ✅ DTs = Medical emergency (mortality up to 15% if untreated). ✅ Benzos are lifesaving (titrate to symptom control). ✅ Give thiamine first to prevent Wernicke’s encephalopathy.

Answer 30

dorsal column and lateral corticospinal column affected risk factor

Answer 31

autoinduction return sezuires in 3-4 weeks promote absent seizures

Answer 32

* A pervasive pattern of disregard for and violation of the rights of others. * Lack of remorse or empathy. * Impulsive and irresponsible behavior. * Deceitfulness and manipulative behavior. * Often violates social norms and laws. Repeatedly lying, stealing, engaging in fights, or failing to hold down a job.

Answer 33

* A pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation. * Strong desire for social interaction, but intense fear of rejection or criticism. * Avoidance of social situations and activities. * Feelings of being socially inept or unappealing. Avoiding social gatherings, holding back in intimate relationships, or fearing criticism.

Answer 34

Optic Neuritis, Transverse Myelitis, Nausea, vomiting, hiccups, and muscle spasms AQP4-IgG antibodies

Answer 35

difficulties in regulating emotions, maintaining relationships, and having a stable sense of self, often leading to impulsive behaviors and a fear of abandonment Intense Fear of Abandonment, Unstable and Intense Relationships, Distorted Sense of Self, Impulsive Behaviors, Emotional Instability, Anger Management Issues, Other Associated Symptoms( Self-harm, Suicidal thoughts or attempts, Dissociation)

Answer 36

a need for admiration from others a grandiose or excessive sense of self-importance a sense of entitlement a preoccupation with themselves a lack of empathy for others. Deny, Dismiss, Devalue & Divorce

Answer 37

* Discomfort when they are not the center of attention * Interaction with others that is inappropriately sexually seductive or provocative * Rapidly shifting and shallow expression of emotions * Consistent use of physical appearance to call attention to themselves * Speech that is extremely impressionistic and vague * Self-dramatization, theatricality, and exaggerated expression of emotion * Suggestibility (easily influenced by others or situations) * Interpretation of relationships as more intimate than they are at leaset 5 of above

Answer 38

A persistent pattern of unstable relationships, self-image, and emotions (ie, emotional dysregulation) and pronounced impulsivity. at least 5 of below * Desperate efforts to avoid abandonment (actual or imagined) * Unstable, intense relationships that alternate between idealizing and devaluing the other person * An unstable self-image or sense of self * Impulsivity in ≥ 2 areas that could harm themselves (eg, unsafe sex, binge eating, reckless driving) * Repeated suicidal behavior and/or gestures or threats or self-mutilation * Rapid changes in mood, lasting usually only a few hours and rarely more than a few days * Persistent feelings of emptiness * Inappropriately intense anger or problems controlling anger * Temporary paranoid thoughts or severe dissociative symptoms triggered by stress * Also, symptoms must have begun by early adulthood but can occur during adolescence.

Answer 39

A persistent, excessive need to be taken of, resulting in submissive and clinging behavior and fears of separation at least 5 of the below * Difficulty making daily decisions without an inordinate amount of advice and reassurance from other people * A need to have others be responsible for most important aspects of their life * Difficulty expressing disagreement with others because they fear loss of support or approval * Difficulty starting projects on their own because they are not confident in their judgment and/or abilities (not because they lack motivation or energy) * Willingness to go to great lengths (eg, do unpleasant tasks) to obtain support from others * Feelings of discomfort or helplessness when they are alone because they fear they cannot take care of themselves * An urgent need to establish a new relationship with someone who will provide care and support when a close relationship ends * Unrealistic preoccupation with fears of being left to take care of themselves

Answer 40

A persistent pattern of preoccupation with order; perfectionism; and control of self, others, and situations 4 of * Preoccupation with details, rules, schedules, organization, and lists * A striving to do something perfectly that interferes with completion of the task * Excessive devotion to work and productivity (not due to financial necessity), resulting in neglect of leisure activities and friends * Excessive conscientiousness, fastidiousness, and inflexibility regarding ethical and moral issues and values * Unwillingness to throw out worn-out or worthless objects, even those with no sentimental value * Reluctance to delegate or work with other people unless those people agree to do things exactly as the patient wants * A miserly approach to spending for themselves and others because they see money as something to be saved for future disasters * Rigidity and stubbornness

Answer 41

A persistent pattern of intense discomfort with and decreased capacity for close relationships 5 of * Ideas of reference (notions that everyday occurrences have special meaning or significance personally intended for or directed to themselves) but not delusions of reference (which are similar but held with greater conviction) * Odd beliefs or magical thinking (eg, believing in clairvoyance, telepathy, or a sixth sense; being preoccupied with paranormal phenomena) * Unusual perceptional experiences (eg, hearing a voice whispering their name) * Odd thought and speech (eg, that is vague, metaphorical, excessively elaborate, or stereotyped) * Suspicions or paranoid thoughts * Incongruous or limited affect * Odd, eccentric, or peculiar behavior and/or appearance * Lack of close friends or confidants, except for 1st-degree relatives * Excessive social anxiety that does not lessen with familiarity and is related mainly to paranoid fears

Answer 42

A severe mental disorder characterized by distortions in thinking, perception, emotions, language, and sense of self.

Answer 43

A personality disorder characterized by a lack of interest in social relationships and a tendency towards a solitary lifestyle.

Answer 44

A mental health condition characterized by a disconnection from reality, which can include hallucinations and delusions.

Answer 45

Hallucinations, delusions.

Answer 46

Social interest.

Answer 47

Reduced ability to form and maintain relationships.

Answer 48

Flat affect.

Answer 49

Medication (antipsychotics) and therapy. olanzapine (atypical antipsycotic ) - reduced extraperamedial side effects, increased risk of weight gain and dyslipidemia

Answer 50

Psychotherapy.

Answer 51

forming relationships.

Answer 52

conductive hearing loss, tinnitus and family history

Answer 53

rare, progressive neurodegenerative disorder affecting both the central and autonomic nervous systems, causing a range of motor and autonomic symptoms

Answer 54

PCS develops after a head injury or concussion, often involving persistent symptoms like headaches, dizziness, and difficulty with concentration and memory

Answer 55

PTSD develops after experiencing or witnessing a traumatic event, such as a serious accident, assault, or natural disaster. persistent nightmares, flashbacks, avoidance behaviors, and hyperarousal, such as feeling easily startled or having difficulty concentrating., Emotional detachment treatment - ssri, snri

Answer 56

Neck pain, numbness/tingling in limbs, weakness, clumsiness, balance issues, and potentially bowel/bladder dysfunction

Answer 57

young female, child baring age, headaches, vision problems (including temporary blindness and double vision), and tinnitus (ringing in the ears) treatment - asetozolamide, carbanic anhydrase inhibitors

Answer 58

Hypocretin/orexin Deficiency

Answer 59

posterior aspect of the frontal lobe in the inferior frontal gyrus non fluent speech, comprehensive ok, repetition impared

Answer 60

ocular pathologies, such as diabetic retinopathy, macular degeneration, or retinal vein occlusion

Answer 61

Wet - 10% worse - Rapid Vision Loss, neovascularization, Dry - Common 90% - early age, Buildup of yellowish deposits (drusen) beneath the retina risk factors - age, family history, smoking, and ethnicity, obese, hypertension Fluorescein angiography

Answer 62

The primary risk factor is a genetic mutation in the NF1 gene, café-au-lait spots, neurofibromas, and in some cases, learning difficulties or behavioral problems, ADHD, Optic pathway glioma, Lisch nodules, Skeletal abnormalities\ causes for hypertension in NF1 - peochromocitoma, renal vasular stenosis, essential hypertension

Answer 63

vestibular schwannomas, leading to hearing loss, tinnitus, and balance problems, with other potential complications including vision problems and neurological deficits

Answer 64

motor nuron disease , subacute degeneration of cords, syringiomialgia

Answer 65

Autosomal recessive, Crm 11, ATM gene mutation rogressive ataxia, telangiectasias (dilated blood vessels, especially on the skin and eyes), recurrent infections due to immune deficiency, and increased risk of cancer (lymphoma) Nervous System: prominent feature - progressive ataxia (loss of coordination),begins in early childhood. chorea, myoclonus, dysarthria, oculomotor apraxia, and neuropathy. Immune System: immunodeficiency, leading to recurrent infections, particularly in the sinuses and lungs, increased risk for certain cancers, especially lymphoma and leukemia. Other Systems: problems with growth, gonadal atrophy, and delayed puberty. Pulmonary problems, including chronic lung damage and chronic otitis with hearing impairment, are also common. Telangiectasias: These are small, dilated blood vessels in the eyes and skin, bladder.

Answer 66

designed to target and block vascular endothelial growth factor (VEGF) signaling, which is crucial for blood vessel formation (angiogenesis)

Answer 67

a rare movement disorder characterized by involuntary, violent, flinging movements on one side of the body Subthalamic Nucleus Damage; basal ganglia

Answer 68

progressive neurodegenerative disorder that affects nerve cells in the brain and spinal cord, leading to muscle weakness and eventually paralysis

Answer 69

Clopidagral + statin

Answer 70

notably angioid streaks and, less commonly, optic neuropathy

Answer 71

perinatal hypoxic brain injury lamotrigin, leverticitam

Answer 72

Clin T - Opthalmopledgia, areflexia, ataxia, anti-GQ1b antibodies intravenous immunoglobulin (IVIg) or plasmapheresis

Answer 73

Waardenburg Syndrome, Sturge-Weber syndrome, Horner's syndrome, and Parry-Romberg syndrome

Answer 74

Progressive muscle weakness, wasting, and twitching, impacting movement, speech, swallowing, and breathing, potentially leading to difficulty with daily activities and emotional lability The short, progressive, purely motor history with upper motor neuron (UMN) and lower motor neuron (LMN) signs is characteristic of motor neurone disease (MND) reflexes and tone variable treatment - riluzole, glutamate antagonist

Answer 75

1st line - lamotregine/ levitiranitam 2nd line - carbamazapine (risk of congenital abnormalities)

Answer 76

A genetic disorder causing kidney disease, hearing loss, and eye abnormalities, can include retinitis pigmentosa (RP) Alport syndrome, RP is often characterized by a "fleck retinopathy" with yellowish or whitish flecks or dots on the retina, progressive vision loss, starting with night vision and peripheral vision, tunnel vision, potential central vision loss

Answer 77

Ischemic events (reduced blood flow, Autoimmune Mechanisms, Antiphospholipid Antibodies

Answer 78

progressive muscle weakness and wasting, primarily in the feet and legs, often leading to foot deformities, difficulty walking, and sensory loss. Type 1 - autosomal dominient

Answer 79

dry mouth, blurred vision

Answer 80

good prognostic factors include younger age at onset, female sex, a relapsing-remitting course, few relapses, complete recovery from relapses, long intervals between relapses, and mainly sensory symptoms poorer prognosis include male sex, older age at onset, motor or cerebellar signs at onset, short intervals between attacks, high relapse rates early in the disease, incomplete remission after initial relapses, and early disability

Answer 81

Bladder disfunction - USS bladder emptying Acute relapse - high dose steriod reduce relapse - natalizumab Spastic Paraparasis - flexes affected more than extensors, lower limb paralysis characterised by peramedal distribution cerebrospinal fluid (CSF) analysis often reveals the presence of oligoclonal bands (OCBs), elevated IgG levels, and a slightly increased white blood cell count A chronic autoimmune, demyelinating disease of the central nervous system (CNS) characterized by inflammatory plaques in the brain, spinal cord, and optic nerves, leading to neurological dysfunction. Key Features 1. Types of MS Type Characteristics Relapsing-Remitting (RRMS) Episodes of worsening (relapses) followed by recovery (most common at diagnosis). Secondary Progressive (SPMS) Gradual worsening after initial relapsing course. Primary Progressive (PPMS) Steady decline from onset (no relapses). Clinically Isolated Syndrome (CIS) First episode suggestive of MS (not yet meeting diagnostic criteria). 3. 2. Common Symptoms Motor: Weakness, spasticity. Sensory: Numbness, paresthesia, Lhermitte’s sign (electric shock sensation with neck flexion). Visual: Optic neuritis (unilateral pain + vision loss). Cerebellar: Ataxia, dysmetria. Bowel/Bladder: Urinary urgency, constipation. Cognitive: Memory loss, slowed processing (later stages). Diagnosis (McDonald Criteria, 2017) 1. MRI Findings T2/FLAIR hyperintensities (periventricular, juxtacortical, infratentorial, spinal cord). Dissemination in space (DIS) and time (DIT): DIS: ≥1 lesion in ≥2 CNS areas. DIT: New lesions on follow-up MRI or simultaneous gadolinium-enhancing + non-enhancing lesions. 2. CSF Analysis Oligoclonal bands (OCBs) (IgG in CSF, not serum). Elevated IgG index. 3. Evoked Potentials Delayed visual evoked potentials (VEPs) in optic neuritis. 4. Differential Diagnosis Mimics: NMOSD, MOGAD, vasculitis, Lyme disease, vitamin B12 deficiency. Management 1. Acute Relapses High-dose IV methylprednisolone (1g/day x 3–5 days). Plasma exchange (PLEX) if steroid-refractory. ✅ Diagnosis requires MRI + clinical/CSF evidence of dissemination in space/time. ✅ Start DMTs early in RRMS to prevent disability. ✅ Ocrelizumab is first FDA-approved for PPMS.

Answer 82

Lateral medullary syndrome (LMS),/ Wallenberg's syndrome or posterior inferior cerebellar artery syndrome vertigo, ataxia, nausea, vomiting, dysphagia, hoarseness, and hiccups, along with sensory loss (pain and temperature) on the ipsilateral face and contralateral body

Answer 83

verapamil - long term prophylaxis pain - around or behind one eye, or in the temple, tearing, redness, and a droopy eyelid, miosis, ptosis ypically presenting with at least five attacks of severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15 minutes to 3 hours (untreated) weith above

Answer 84

temporal lobe

Answer 85

dopamine agonist cts on G-protein-coupled inhibitory neurons, inhibiting adenylyl cyclase and calcium channels while activating potassium channels.

Answer 86

Caused by reduced blood flow to the anterior two-thirds of the spinal cord, results in motor deficits and loss of pain/temperature sensation,

Answer 87

Optic atrophy occurs when the axons of the retinal ganglion cells (RGCs), which form the optic nerve, die or are damaged. ischemia, inflammation, compression, toxic exposure, trauma, and hereditary conditions, Glaucoma, multiple sclerosis, drugs (Ethambutol, Amiodarone, Linezolid, isoniazid, chloramphenicol, ciprofloxacin

Answer 88

Antibiotics: Sulfonamides, including trimethoprim-sulfamethoxazole, are frequently implicated. Anticonvulsants: Lamotrigine, carbamazepine, phenytoin, and phenobarbitone are known triggers. Pain Relievers: Acetaminophen (Tylenol), ibuprofen (Advil, Motrin IB), and naproxen sodium (Aleve) have been linked to SJS. Other Medications: Allopurinol (used for gout), nevirapine (an antiretroviral), and certain non-steroidal anti-inflammatory drugs (NSAIDs) can also trigger SJS. 2. Infections: Viral Infections: Herpes, mumps, flu, and the Epstein-Barr virus are potential triggers, especially in children. Bacterial Infections: Mycoplasma pneumoniae and cytomegalovirus have also been linked to SJS. 3. Other Factors: Graft-versus-host disease: This can occur after a stem cell transplant. Certain genes: Variations in genes, particularly those related to the human leukocyte antigen (HLA) complex, can increase the risk. Weakened Immune System: Conditions like HIV/AIDS

Answer 89

tenous low density changes within teh reigion of anterioa and medial temporal lobe and island of reil

Answer 90

always in immunosuppresion

Answer 91

MRI / CT classical bilateral thalamic involvement

Answer 92

Autoimune short term memory involved, seizures, psych symptoms

Answer 93

progressive degeneration of photoreceptor cells (rods and cones) in the retina Nyctalopia, gradual narrowing of their visual field, leading to tunnel vision, Reduced Visual Acuity,

Answer 94

' present as drunk' Dysdiadochokinesia Ataxia (gait and posture) Nystagmus Intention tremor Slurred, staccato speech Hypotonia/heel-shin test DANISH

Answer 95

neurological symptoms originating from the brainstem, such as vertigo, slurred speech, and double vision, often preceding or accompanying a headache.

Answer 96

ausing stroke and other neurological problems due to damage to small blood vessels in the brain, often leading to migraines, cognitive decline, and psychiatric disturbances. NOTCH3 gene, which is located on chromosome 19

Answer 97

characterized by sudden, brief, shock-like jerks or twitches of a muscle or muscle group, often occurring in clusters and sometimes mistaken for clumsiness Treatment - sadium valporate

Answer 98

trans-synaptic degeneration of the inferior olivary nucleus (ION) in the brainstem, often resulting from lesions in the Guillain-Mollaret triangle (GMT). HOD is characterized by hypertrophy (enlargement) of the ION, rather than atrophy, and can present with symptoms like palatal tremor, nystagmus, and ataxia

Answer 99

Larger than normal, dilated pupil. diluted pilocarpine drops, where the affected pupil constricts more than the normal pupil. Light Response: Slow or absent constriction to light (both direct and consensual). Near Response: Intact and often slow constriction to near stimuli. Cause: Damage to the post-ganglionic parasympathetic fibers. Associated Conditions: Benign peripheral neuropathy

Answer 100

Appearance: Small, constricted pupils. Light Response: Poor or absent constriction to light. Near Response: Normal or brisk constriction to near stimuli. Associated Conditions: Characteristic finding in neurosyphilis (late-stage syphilis). Cause: Interference with the light reflex pathway. Other Characteristics: Irregular pupil shape (oval, egg-shaped, tear-shaped, etc.). Distinguishing Features: AR pupils are small and misshapen, while Adie's tonic pupils remain dilated. Mnemonic: "Accommodate but do not react".

Answer 101

Na loss is accomponied by water loss, high urin output , normal kidney function, fluid dpletion

Answer 102

Mania and hypomania are both characterized by elevated mood and increased energy, but mania is more severe, potentially causing significant impairment and requiring hospitalization, while hypomania is milder and doesn't typically lead to such disruptions. Here's a more detailed comparison: Similarities: Elevated Mood: Both involve periods of abnormally and persistently elevated, expansive, or irritable mood. Increased Energy: Both are associated with increased activity or energy levels. Increased Talkativeness: Both can involve being more talkative than usual, with rapid and pressured speech. Racing Thoughts: Both can include racing thoughts or jumping quickly from one topic to another. Distractibility: Both can involve being easily distracted. Decreased need for sleep Bipolar I: 1+ manic episodes. Bipolar II: 1+ hypomanic + 1+ major depressive episodes. Rule out: Substance-induced mania (cocaine, steroids). Medical causes (hyperthyroidism, brain tumors). ✅ Mania is a symptom; bipolar disorder is the illness. ✅ Bipolar I = mania; Bipolar II = hypomania + depression. ✅ Hypomania is less severe than mania (no hospitalization needed).

Answer 103

caused by nerve damage during birth, fall from tree Weakness or paralysis in the forearm, wrist, and hand. "Claw hand", stiff joints c8 - T1

Answer 104

c5-6 weakness in deltoid, biceps, infraspinatus

Answer 105

euroanatomy & Physiology Primary Pathway: Sensory input (touch, proprioception) → Dorsal columns (gracile/cuneate fasciculi) → Medial lemniscus → Thalamus (VPL nucleus) → Primary somatosensory cortex (postcentral gyrus, areas 3,1,2) → Secondary somatosensory cortex & parietal association areas. Key Brain Regions: Parietal lobe (especially supramarginal gyrus) – Integrates tactile and spatial information. Corpus callosum – Allows interhemispheric transfer for bilateral comparison. Clinical Significance Loss of stereognosis (astereognosis) suggests parietal lobe dysfunction (e.g., stroke, tumor, neurodegenerative disease). Unilateral impairment → Contralateral parietal lesion. Bilateral impairment → Diffuse cortical dysfunction (e.g., dementia, advanced multiple sclerosis).

Answer 106

a neurological condition characterized by unilateral optic atrophy (vision loss) in one eye and papilledema (swelling of the optic disc) in the other, often caused by a mass lesion, such as a tumor, in the frontal lobe

Answer 107

Foreign body sensation in the eye. Eye pain. Sensitivity to light. Watery eyes.

Answer 108

Brown-Séquard syndrome, caused by a spinal cord hemisection, results in a unique pattern of motor and sensory deficits. On the same side of the injury (ipsilateral), there's motor weakness or paralysis, and loss of proprioception, vibration sense, and fine touch. On the opposite side of the injury (contralateral), there's a loss of pain and temperature sensation Affected Tracts: Ipsilateral (same side as lesion): Corticospinal tract → motor weakness (UMN signs). Dorsal columns → loss of vibration/proprioception. Contralateral (opposite side): Spinothalamic tract → loss of pain/temperature (decussates 1–2 levels above entry). ✅ Ipsilateral UMN weakness + dorsal column loss + contralateral spinothalamic loss. ✅ LMN signs at lesion level (e.g., areflexia). ✅ MRI spine urgent to identify reversible causes (e.g., tumor). Management Surgical decompression (if compressive lesion, e.g., tumor, hematoma). High-dose steroids (if inflammatory, e.g., MS flare). Physical therapy (rehabilitation for weakness). Prognosis Partial recovery possible with early intervention. Permanent deficits common if severe/cause is irreversible (e.g., infarction).

Answer 109

The combination of headache, increasing drowsiness (suggesting increasing intracranial pressure), focal neurological signs and seizures in a woman shortly post partum is highly suggestive of a venous sinus thrombosis. Seizures: Common, 40% of patients with CVST Headache- 90% Focal Neurological Deficits, Altered Mental Status, proptosis, chemosis, and cranial nerve palsies Pulsatile Tinnitus papilledema, visual changes, and headaches that worsen with Valsalva maneuvers (straining) - raised ICP Def Diagnosis - MRV

Answer 110

X-linked recessive - mutation in the androgen receptor (AR) gene, specifically an expansion of a CAG trinucleotide repeat. causes progressive degeneration of lower motor neurons, leading to muscle weakness and atrophy Progressive Muscle Weakness: Weakness begins in adulthood, typically between 30 and 50, and progresses slowly over time. Muscle Atrophy: Affected muscles shrink due to disuse. Fasciculations: Muscle twitches are common. Bulbar Dysfunction: Difficulty with swallowing and speech due to weakness in the face and throat muscles. Androgen Insensitivity: Some males experience gynecomastia, testicular atrophy, and reduced fertility. Slow Progression: SBMA progresses slowly over decades, allowing for a relatively normal lifespan.

Answer 111

a condition where a fluid-filled cavity, called a syrinx, within the spinal cord extends up to the brainstem, particularly the medulla oblongata. This can affect the brainstem and cranial nerves, leading to a range of neurological symptoms, including facial palsy. Syrinx: A fluid-filled cavity within the spinal cord. Brainstem Extension: The syrinx extends upwards into the brainstem, often the medulla oblongata. Neurological Symptoms: Affected cranial nerves can cause facial palsies, and other neurological symptoms may include sensory and motor deficits, dysphagia, and respiratory problems. associations Chiari Malformation Communicating Syringomyelia: The cavity may communicate with the fourth ventricle. Spinal Cord Injury

Answer 112

Haloperidol is a D2-receptor antagonist. It has a central antiemetic action, binding to receptors in the area postrema, which is a medullary structure controlling vomiting.

Answer 113

a group of neurological disorders where the body's immune system mistakenly attacks the brain, causing inflammation. This inflammation can lead to various symptoms, including memory loss, psychosis, changes in thinking and behavior, and seizures Clinical Features Common Symptoms Psychiatric: Agitation, hallucinations, catatonia (mimicking schizophrenia). Neurologic: Seizures, movement disorders (orofacial dyskinesias in NMDAR), memory loss. Autonomic: Hyperthermia, tachycardia, hypotension (NMDAR). Red Flags for AIE ✔ Rapid-onset psychosis (days-weeks). ✔ Seizures refractory to antiepileptics. ✔ FBDS (LGI1) or orofacial dyskinesias (NMDAR). B. Key Tests Test Findings CSF Lymphocytic pleocytosis, elevated IgG index, oligoclonal bands. MRI Brain Medial temporal lobe hyperintensities (LGI1, NMDAR), or normal. EEG Extreme delta brush (NMDAR), epileptiform discharges. Antibody panels Serum/CSF testing for neuronal antibodies (Cell-based assays preferred). PET/CT Screen for occult malignancy (if paraneoplastic suspected). C. Differential Diagnosis Condition Key Differentiator Viral encephalitis (HSV) Fever, PCR+ CSF. Creutzfeldt-Jakob disease Rapid dementia, 14-3-3 protein, MRI DWI hyperintensities. Psychiatric disorders Chronic course, no seizures/autonomic dysfunction. ✔ Test for neuronal antibodies (CSF + serum). ✔ Treat early (steroids + IVIG/rituximab). ✔ Screen for tumors (especially in NMDAR/LGI1).

Answer 114

It results in confused thinking and a lack of awareness of someone's surroundings. The disorder usually comes on fast — within hours or a few days. Delirium can often be traced to one or more factors . Key Features of Delirium Acute onset (hours to days) with waxing and waning symptoms. Impaired attention (e.g., difficulty focusing or following conversations). Disorganized thinking (illogical speech, confusion). Altered consciousness (hyperactive, hypoactive, or mixed subtypes). 2. Types of Delirium Subtype Characteristics Common Causes Hyperactive Agitation, hallucinations, restlessness Alcohol withdrawal, drug toxicity Hypoactive Lethargy, drowsiness, reduced movement Metabolic disturbances, sepsis Mixed Fluctuates between hyperactive and hypoactive Multiple contributing factors ✅ Delirium is a medical emergency—always search for the cause. ✅ Hypoactive delirium is often missed (mistaken for depression/dementia). ✅ Antipsychotics are second-line (non-drug interventions first). Avoid routine use of antipsychotics (e.g., haloperidol) unless agitation poses safety risks or non-pharmacological measures fail Benzodiazepines are contraindicated except for alcohol/benzodiazepine withdrawal. Dexmedetomidine may be considered in critical care for sedation over other agents

Answer 115

Alzheimer’s disease is a progressive neurodegenerative disorder and the most common cause of dementia (60-80% of cases). It is characterized by memory loss, cognitive decline, and behavioral changes due to brain cell degeneration. Key Features Gradual onset with worsening memory impairment (initially short-term memory loss). Pathological hallmarks: Amyloid plaques (Aβ protein aggregates). Neurofibrillary tangles (tau protein hyperphosphorylation). Neuronal loss (especially in hippocampus & cortex). No cure, but treatments can slow progression. Causes & Risk Factors A. Non-Modifiable Age (biggest risk factor; >65 yrs, doubles every 5 years after). Genetics: APOE-e4 allele (increases risk, not deterministic). Familial AD (rare, <1%): Mutations in APP, PSEN1, PSEN2 (early-onset, 30s-50s). B. Modifiable (Potential Prevention Targets) Cardiovascular risks (hypertension, diabetes, obesity). Lifestyle: Smoking, physical inactivity, poor diet. Traumatic brain injury (TBI). Medications (Symptom Management) Drug Class Examples Effect Cholinesterase inhibitors Donepezil, Rivastigmine, Galantamine Improve memory/attention (mild-moderate AD). NMDA antagonist Memantine Slows cognitive decline (moderate-severe AD). Anti-amyloid monoclonal antibodies (New!) Aducanumab, Lecanemab Reduce amyloid plaq Differential Diagnosis Vascular dementia (stepwise decline, stroke history). Lewy body dementia (visual hallucinations, parkinsonism). Frontotemporal dementia (personality changes first).

Answer 116

Orbital apex syndrome (OAS) is a rare but vision-threatening condition caused by compression or inflammation of structures in the orbital apex, leading to multiple cranial nerve palsies and potential blindness. Urgent diagnosis and treatment are critical to prevent permanent damage. The orbital apex is a critical area where the following structures converge: Cranial nerves: CN II (Optic nerve) → Vision. CN III (Oculomotor) → Eye movement (medial, superior, inferior rectus; levator palpebrae). CN IV (Trochlear) → Superior oblique muscle. CN VI (Abducens) → Lateral rectus muscle. CN V1 (Ophthalmic branch of trigeminal) → Corneal sensation. Blood vessels: Ophthalmic artery/vein. Inflammatory Sarcoidosis, IgG4-related disease, Tolosa-Hunt syndrome Infectious Fungal (mucormycosis, aspergillosis), bacterial (sinusitis, TB) Neoplastic Metastasis (breast, lung), lymphoma, meningioma Trauma Fractures, hematoma Vascular Aneurysm, carotid-cavernous fistula Symptoms & Signs Painful ophthalmoplegia (common in inflammatory causes). Vision loss (optic nerve compression → irreversible if untreated). Ptosis (CN III palsy). Proptosis (if mass lesion present). Pupillary dysfunction (afferent pupillary defect if CN II affected). Sensory loss (CN V1 involvement → reduced corneal reflex). ✅ Think OAS in any patient with painful ophthalmoplegia + vision loss. ✅ MRI with contrast is the best diagnostic tool. ✅ Steroids for inflammation, antifungals for infection, surgery for tumors. ✅ Time-sensitive condition → urgent referral to ophthalmology/neurology.

Answer 117

is a rare condition caused by the compression or damage to structures passing through the superior orbital fissure, a bony cleft at the apex of the orbit. It leads to multiple cranial nerve palsies and ocular symptoms. Structures Involved: The superior orbital fissure transmits: Cranial Nerves: Oculomotor nerve (CN III) – Controls most extraocular muscles (except LR6, SO4). Trochlear nerve (CN IV) – Innervates the superior oblique muscle. Abducens nerve (CN VI) – Innervates the lateral rectus muscle. Ophthalmic branch of trigeminal nerve (V1) – Provides sensory innervation to the eye and forehead. Sympathetic fibers (from the carotid plexus). Superior ophthalmic vein – Drains blood from the orbit. Differential Diagnosis: Orbital Apex Syndrome (similar but also includes optic nerve (CN II) involvement → vision loss). Cavernous Sinus Syndrome (more posterior, may involve CN V2 and Horner’s syndrome). Myasthenia Gravis (fluctuating weakness, no sensory loss).

Answer 118

Cavernous sinus thrombosis (CST) is a life-threatening condition caused by thrombosis (blood clot) and infection within the cavernous sinus, a venous structure at the base of the brain. It is a rare but serious complication of infections in the face, sinuses, ears, or orbits. Clinical Features Early Symptoms (Unilateral, may become bilateral): Fever, headache, periorbital edema. Eye findings: Proptosis (bulging eye). Chemosis (conjunctival swelling). Ptosis. Ophthalmoplegia (CN III, IV, VI palsy → double vision). Pupillary abnormalities (dilated or fixed if CN III affected). Retinal venous engorgement. Sensory loss (CN V1/V2 involvement → forehead/cheek numbness). Late Symptoms (if untreated): Bilateral involvement (sinuses communicate). Meningitis, sepsis, brain abscess. Pituitary dysfunction (due to compression). Diagnosis Imaging: MRI + MRV (gold standard) → shows thrombosis, sinus inflammation. CST is a medical emergency! Think of it in patients with fever, eye swelling, and cranial nerve palsies. MRI + MRV is diagnostic. Treat aggressively with IV antibiotics ± anticoagulation.

Answer 119

Both lead poisoning and acute intermittent porphyria (AIP) can present with abdominal pain, neuropathy, and psychiatric symptoms, making them important differential diagnoses. However, their underlying causes, lab findings, and treatments differ significantly. Both can cause abdominal pain + neuropathy. Lead poisoning: Look for exposure history, anemia, basophilic stippling, ↑ blood lead. AIP: Look for pink urine, ↑ PBG/ALA, triggered by drugs/fasting. Misdiagnosis risk: AIP is often mistaken for surgical abdomen or psychiatric illness.

Answer 120

✅ Levels >1.5 mEq/L → Neurological symptoms. ✅ HD for severe toxicity (coma, seizures, levels >2.5–4.0 mEq/L). ✅ Chronic toxicity can occur at lower levels. mptoms depend on serum lithium levels and chronicity: Lithium Level Symptoms 1.2–1.5 mEq/L (Mild) Tremor, nausea, polyuria, mild confusion. 1.5–2.5 mEq/L (Moderate) Worsening confusion, ataxia, hyperreflexia, myoclonus, seizures. >2.5 mEq/L (Severe) Coma, seizures, arrhythmias (QT prolongation, bradycardia), renal failure. Chronic Toxicity Features More neurotoxicity at lower levels (e.g., confusion at 1.5 mEq/L). Irreversible cerebellar damage (if prolonged exposure). Diagnosis Serum lithium level (check 12 hrs post-dose for chronic toxicity). Electrolytes & Renal Function: Hyponatremia (worsens toxicity). Elevated creatinine (lithium-induced nephrogenic DI). ECG: QT prolongation, T-wave flattening, bradycardia. Neurological Exam: Hyperreflexia, clonus, ataxia, dysarthria.

Answer 121

Medical Therapy (All Patients) Anti-platelets: Aspirin 81–325 mg/day (first-line). Clopidogrel (if aspirin-intolerant). Risk Factor Control: Statin (high-intensity, e.g., atorvastatin 40–80 mg). BP control (goal <130/80 mmHg). Smoking cessation, diabetes management. CEA (Carotid Endarterectomy) Symptomatic ≥50%, asymptomatic ≥70% Gold standard; durable but invasive CAS (Carotid Artery Stenting) High surgical risk, younger patients Less invasive; higher peri-op stroke risk

Answer 122

Pharmacological Treatment A. Dopaminergic Therapies (1) Levodopa (L-DOPA) + Carbidopa (Sinemet®) Gold standard for motor symptoms (bradykinesia, rigidity, tremor). Carbidopa prevents peripheral conversion to dopamine (reduces nausea). Dosing: Start low (e.g., 25/100 mg TID), escalate as needed. Side Effects: Motor fluctuations ("wearing-off," dyskinesias) after 5+ years. Psychosis (hallucinations, confusion). (2) Dopamine Agonists (DA) Pramipexole, Ropinirole, Rotigotine (patch). Used early (young patients) to delay levodopa. Side Effects: Impulse control disorders (gambling, hypersexuality). Edema, somnolence. (3) MAO-B Inhibitors Selegiline, Rasagiline. Mild symptomatic benefit, may slow progression. (4) COMT Inhibitors Entacapone, Tolcapone (prolong levodopa effect). Used for "wearing-off" phenomena. (5) Amantadine Reduces dyskinesias (NMDA antagonist). B. Non-Motor Symptom Management Symptom Treatment Psychosis Quetiapine, Clozapine (avoid typical antipsychotics). Depression SSRIs (e.g., Sertraline). Dementia Rivastigmine (AChE inhibitor). Constipation Polyethylene glycol (Miralax®). Orthostatic Hypotension Fludrocortisone, Midodrine. Apomorphine is a medication that treats certain episodes of Parkinson's disease that affect your ability to move Excessive sleepiness - Modafin ✅ Levodopa = most effective, but delayed to reduce long-term complications. ✅ Dopamine agonists = first-line in younger patients. ✅ DBS = option for refractory motor fluctuations. ✅ Non-motor symptoms (e.g., depression, psychosis) require targeted therapy.

Answer 123

✅ AN = Underweight + restriction → Cardiac/bone risks. ✅ BN = Normal weight + binge/purge → Electrolyte/dental risks. ✅ Both require multidisciplinary care (medical, nutritional, psychological).

Answer 124

First-Line Investigations: Bloods: FBC, CRP, U&E, LFTs, glucose, blood cultures. Neuroimaging: MRI brain (preferred) – Temporal lobe hyperintensity (HSV). CT head (if MRI delayed) – Rule out mass lesion/bleed. Lumbar puncture (LP): CSF PCR for HSV-1/2, VZV, enterovirus, others. CSF opening pressure, cell count, protein, glucose. Contraindications: ↑ICP, coagulopathy, thrombocytopenia. 2. Empiric Treatment (Start Immediately) Antiviral Therapy: Aciclovir IV (10 mg/kg 8-hourly) Duration: Minimum 14–21 days (HSV/VZV). Adjust dose for renal impairment. Add antibiotics (e.g., ceftriaxone) if bacterial meningitis possible. If Immunocompromised: Consider broader coverage (e.g., ganciclovir for CMV, foscarnet for HHV-6). 3. Adjunctive Therapies Seizures: Levetiracetam/lorazepam (avoid enzyme-inducers like phenytoin). Raised ICP: Mannitol/hypertonic saline, elevate head. Steroids (controversial): Consider in ADEM or autoimmune encephalitis. 4. Confirmatory Testing & De-escalation Positive HSV/VZV PCR: Continue aciclovir. Negative PCR + improving: Consider stopping at 10 days if low suspicion. Autoimmune encephalitis suspected: Send NMDA-R/other autoantibodies

Answer 125

Central (Brainstem/Cerebellar) Nystagmus 1. Gaze-Evoked Nystagmus Cause: Cerebellar/brainstem lesion (MS, stroke). Features: Beats in direction of gaze (e.g., right gaze → right-beating). 2. Downbeat Nystagmus Cause: Craniocervical junction lesions (Chiari malformation, Mg²⁺ deficiency). Features: Fast phase downward (worse on lateral gaze). 3. Upbeat Nystagmus Cause: Medullary (e.g., stroke, Wernicke’s). Features: Fast phase upward. 4. See-Saw Nystagmus Cause: Parasellar lesions (e.g., pituitary tumor). Features: One eye elevates/intorts while other depresses/extorts. 5. Convergence-Retraction Nystagmus Cause: Dorsal midbrain (Parinaud’s syndrome). Features: Eyes jerk inward during upward gaze attempt. 6. Periodic Alternating Nystagmus (PAN) Cause: Cerebellar nodulus lesions (e.g., ataxia-telangiectasia). Features: Direction reverses every 2–3 minutes. ✅ Peripheral: Unidirectional, suppressed by fixation, torsional. ✅ Central: Bidirectional, pure vertical, no fixation suppression. ✅ Cerebellum: Downbeat, gaze-evoked. ✅ Midbrain: Convergence-retraction, see-saw.

Answer 126

Somatic Symptom Disorder (SSD) ≥1 distressing somatic symptom + excessive thoughts/behaviors about it. Example: Chronic pain with catastrophic thinking. Illness Anxiety Disorder (IAD) Preoccupation with having a serious illness without prominent somatic symptoms. Example: "I’m sure this headache is a brain tumor" (despite normal MRI). Conversion Disorder (Functional Neurological Symptom Disorder) Neurologic symptoms (e.g., paralysis, seizures) incompatible with medical conditions. Example: Arm weakness after stressor, but normal EMG. Factitious Disorder Intentional symptom fabrication to assume the "sick role" (no external reward). Munchausen syndrome: Severe form with hospital-seeking behavior. Malingering (Not a mental disorder) Feigning symptoms for external gain (e.g., disability benefits).

Answer 127

An autosomal dominant neurocutaneous disorder caused by mutations in TSC1 (hamartin) or TSC2 (tuberin) genes, leading to mTOR pathway overactivation and benign tumor growth in multiple organs (brain, skin, heart, kidneys, lungs). Clinical Features 1. Neurological (80–90% of patients) Cortical tubers (developmental brain malformations → epilepsy, intellectual disability). Subependymal nodules (SENs) (along ventricles, often calcified). Subependymal giant cell astrocytoma (SEGA) (10–15%, risk of hydrocephalus). Epilepsy (infantile spasms, focal seizures). 2. Dermatologic (90%) Hypomelanotic macules ("ash-leaf spots," Wood’s lamp enhances). Facial angiofibromas (adenoma sebaceum, nose/cheeks). Shagreen patch (leathery plaque on lower back). Ungual fibromas (periungual or subungual). 3. Systemic Involvement Renal: Angiomyolipomas (40–80%, risk of hemorrhage), renal cysts. Cardiac: Rhabdomyomas (60% infants, often regress with age). Pulmonary: Lymphangioleiomyomatosis (LAM, women > men). Ocular: Retinal hamartomas (50%). ✅ Triad: Seizures + intellectual disability + facial angiofibromas (but variable expressivity). ✅ mTOR inhibitors (everolimus) are disease-modifying. ✅ Screen for SEGA, renal, and pulmonary complications.

Answer 128

Symptoms During Episodes: Motor: Asynchronous limb movements ("thrashing"), side-to-side head movements, pelvic thrusting. Verbal: Crying, shouting, or speaking during the episode. Eyes: Typically closed (vs. epileptic seizures, where eyes are often open). Duration: Often longer than epileptic seizures (>2 minutes). Post-ictal state: Rapid recovery or persistent fatigue without confusion. Key Takeaways ✅ Diagnosis requires video-EEG to rule out epilepsy. ✅ Closed eyes + asynchronous movements = red flags for PNES. ✅ CBT is the cornerstone of treatment.

Answer 129

A progressive neurodegenerative disorder characterized by alpha-synuclein protein aggregates (Lewy bodies) in the cortex and brainstem. It shares features with both Alzheimer’s disease (AD) and Parkinson’s disease (PD). Core Symptoms (DLB Diagnostic Criteria – ≥2 for Probable DLB) Fluctuating cognition (e.g., attention/alertness varies hourly/daily). Recurrent visual hallucinations (detailed, often of people/animals). Parkinsonism (bradykinesia, rigidity, gait instability; tremor less prominent than in PD). REM Sleep Behavior Disorder (RBD) (acting out dreams, often years before dementia). Supportive Features Severe neuroleptic sensitivity (worsens parkinsonism). Autonomic dysfunction (orthostatic hypotension, urinary incontinence). Depression, apathy, delusions. 1. Cognitive Symptoms Cholinesterase Inhibitors (donepezil, rivastigmine): First-line for cognition/behavior. Memantine: May help in moderate-severe LBD. 2. Motor Symptoms Levodopa: Low doses (improves parkinsonism but may worsen hallucinations). Avoid dopamine agonists (high psychosis risk). 3. Psychiatric Symptoms Atypical antipsychotics (quetiapine, clozapine) if absolutely necessary (caution: high sensitivity). Avoid typical antipsychotics (e.g., haloperidol → severe rigidity, death). ✅ Fluctuating cognition + visual hallucinations + RBD = Think LBD. ✅ Treat with cholinesterase inhibitors first; avoid antipsychotics. ✅ DaTscan helps distinguish from AD but not from PDD.

Answer 130

known as gyrate atrophy of the choroid and retina (GACR), is a rare, autosomal recessive disorder characterized by progressive vision loss due to retinal degeneration. It's caused by a deficiency of the enzyme ornithine aminotransferase, leading to elevated levels of ornithine in the blood. presents with progressive chorioretinal degeneration, myopia, night blindness, and eventually complete blindness in the fourth or fifth decade.

Answer 131

A life-threatening, drug-induced movement disorder caused by dopamine receptor blockade (typically antipsychotics), characterized by hyperthermia, rigidity, altered mental status, and autonomic instability. 1. Common Triggers Antipsychotics: Typical (haloperidol > fluphenazine). Atypical (risperidone, olanzapine). Other dopamine antagonists: Metoclopramide, prochlorperazine. Rapid dose escalation or high-potency agents. 2. Risk Factors Dehydration, agitation, iron deficiency, catatonia. Clinical Features (Classic Tetrad) Fever (>38°C, often >40°C). Muscle rigidity ("lead-pipe" rigidity, severe). Altered mental status (delirium → coma). Autonomic dysfunction (tachycardia, labile BP, diaphoresis). Supportive Signs: Elevated CK (rhabdomyolysis, often >1,000 IU/L). Leukocytosis (WBC >15,000/mm³). Metabolic acidosis. Diagnosis 1. Labs & Imaging CK (markedly elevated). Electrolytes (hyperkalemia, AKI from rhabdo). Urinalysis (myoglobinuria). Exclude infections (blood/CSF cultures, chest X-ray). 2. Differential Diagnosis Condition Key Distinctions Serotonin syndrome Hyperreflexia, clonus, diarrhea (SSRIs/MAOIs). Malignant hyperthermia Succinylcholine/halogenated anesthetics. Catatonia No fever/CK rise, may precede NMS. ✅ NMS = Fever + rigidity + autonomic instability + elevated CK. ✅ Stop antipsychotics, cool, hydrate, dantrolene/bromocriptine. ✅ Distinguish from serotonin syndrome (hyperreflexia/clonus vs. rigidity).

Answer 132

Conus Medullaris: Trauma (e.g., T12–L2 fracture). Spinal tumors (e.g., ependymoma). Infarction (e.g., anterior spinal artery occlusion). Cauda Equina: Herniated disc (L4–L5, L5–S1 most common). Spinal stenosis, tumors, abscess. Diagnostic Workup MRI spine (emergency): Gold standard for both. CT myelogram (if MRI unavailable). Bladder scan (post-void residual >200 mL suggests dysfunction). ✅ Conus = Cord injury → early bladder retention, hyperreflexia. ✅ Cauda Equina = Nerve root injury → radicular pain, areflexia, late incontinence. ✅ Both need emergency MRI, but cauda equina requires faster surgery.

Answer 133

forms: sporadic (most common), variant (linked to BSE), familial/inherited, and iatrogenic (transmitted through medical procedures) Sporadic (sCJD): Most common (85–90% of cases), no known cause, typically affects ages 55–75 Genetic/Familial (fCJD): 10–15% of cases, linked to mutations in the PRNP gene (e.g., E200K) Iatrogenic (iCJD): Rare (<1%), caused by exposure to infected tissues during medical procedures (e.g., corneal transplants, contaminated surgical instruments) Variant (vCJD): Linked to consuming meat from cattle with bovine spongiform encephalopathy (BSE); younger onset (teens–30s) and longer duration Early stage: Memory loss, mood changes, ataxia, visual disturbances, and psychiatric symptoms (e.g., depression, hallucinations) Advanced stage: Rapid dementia, myoclonus (muscle jerks), rigidity, blindness, and akinetic mutism. Death typically occurs within 4–12 months (70% within a year) vCJD distinct features: Early psychiatric symptoms, sensory abnormalities, and longer survival (~14 months) Diagnosis Clinical assessment: Rapid cognitive decline + myoclonus or ataxia Tests: MRI: Hyperintensity in basal ganglia or cortical ribboning (90% sensitivity) EEG: Periodic sharp-wave complexes (50–60% of sCJD cases) CSF analysis: Elevated 14-3-3 and tau proteins (non-specific); RT-QuIC (real-time quaking-induced conversion) detects prions with >80% sensitivity Definitive diagnosis: Brain biopsy or postmortem examination Causes and Transmission Prion mechanism: Misfolded prion proteins (PrP^Sc) convert normal proteins (PrP^C) into toxic aggregates, leading to neuronal death Transmission routes: Iatrogenic: Contaminated surgical instruments, grafts, or human growth hormone. Dietary (vCJD): BSE-infected beef Familial: Autosomal-dominant PRNP mutations No evidence of casual contact or blood transfusion transmission (except vCJD)

Answer 134

1. Fluent Aphasias (Wernicke’s Area & Posterior Language Areas) Speech is fluent but often nonsensical due to poor comprehension. a) Wernicke’s Aphasia (Receptive Aphasia) Location of Damage: Wernicke’s area (posterior superior temporal gyrus). Speech: Fluent but paraphasic errors (word substitutions, neologisms). "Word salad" – sentences lack meaning. Comprehension: Severely impaired. Repetition: Poor. Example: "The telfon is blipping in the vorpal snark." b) Conduction Aphasia Location of Damage: Arcuate fasciculus (connection between Broca’s & Wernicke’s areas). Speech: Fluent but frequent phonemic paraphasias (e.g., "television" → "televisop"). Comprehension: Intact. Repetition: Severely impaired (hallmark feature). Example: "I wanted to ride the bicycle… no, bictory… bictoride… bike." c) Transcortical Sensory Aphasia Location of Damage: Posterior parietotemporal region (spares Wernicke’s but disconnects it). Speech: Fluent but nonsensical (similar to Wernicke’s). Comprehension: Poor. Repetition: Preserved (key difference from Wernicke’s). Example: "The thing is over there… what’s it called?" 2. Non-Fluent Aphasias (Broca’s Area & Frontal Lobe) Speech is effortful, slow, and grammatically simplified. a) Broca’s Aphasia (Expressive Aphasia) Location of Damage: Broca’s area (posterior inferior frontal gyrus). Speech: Non-fluent, telegraphic (omits small words: "go store"). Agrammatism (lack of grammar). Comprehension: Mostly intact. Repetition: Impaired. Example: "Walk… dog… park… yes." b) Global Aphasia Location of Damage: Large left perisylvian region (Broca’s + Wernicke’s + arcuate fasciculus). Speech: Severely non-fluent, few words. Comprehension: Poor. Repetition: Impaired. Example: "No… no… no talk." c) Transcortical Motor Aphasia Location of Damage: Anterior/superior to Broca’s area (supplementary motor area). Speech: Non-fluent, slow initiation. Comprehension: Intact. Repetition: Preserved (key difference from Broca’s). Example: "I… can’t… speak… but… yes." 3. Other Aphasias a) Anomic Aphasia Location of Damage: Angular gyrus or temporal lobe. Speech: Fluent but word-finding difficulty (circumlocutions). Comprehension: Intact. Repetition: Intact. Example: "I was using the… uh… thing to cut the… you know, the food." b) Mixed Transcortical Aphasia (Isolation Aphasia) Location of Damage: Watershed areas (spares perisylvian language zones). Speech: Minimal spontaneous speech, may echolalia (repeat others). Comprehension: Poor. Repetition: Preserved (only language function intact). Example: "What did you say? Say it again?" Summary Table of Aphasia Types Type Fluent? Comprehension Repetition Speech Pattern Wernicke’s Yes Poor Poor Word salad, paraphasias Broca’s No Intact Poor Telegraphic, agrammatic Conduction Yes Intact Poor Phonemic paraphasias Global No Poor Poor Very limited speech Transcortical Motor No Intact Intact Non-fluent, hesitant Transcortical Sensory Yes Poor Intact Fluent but empty Mixed Transcortical Minimal Poor Intact Echolalia Anomic Yes Intact Intact Word-finding pauses Key Points Fluent vs. Non-Fluent → Determines if speech flows naturally. Comprehension → Wernicke’s area damage impairs understanding. Repetition → Arcuate fasciculus damage disrupts repetition (except in transcortical aphasias).

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