Flashcards in NB 2 CRAM Deck (117):
Cause: Lesion of PPRF & MLF on one side due to infarction ormultiple sclerosisSymptoms: Inability of ipsilater eye to perform horizonal eye movements & of contralateral eye to adduct normally (usually exhibiting nystagmus on terminal abduction)
Symptoms: Develop 3-8 hours after they are deprived from alcohol. Increased NorE (Hyperhidrosis, tachycardia, hypertension, tremor). Increased dopamine (psychotic symptoms). Increased glutamate (epileptic seizures). Withdrawal symptoms typically last 5-7 days. 5% develop delirium 2-3 days after they've stopped drinking & in some cases it can be fatal.
Cause: Due to toxic effect of alcohol or associated nutritional deficiency (e.g. B1 [thiamin] deficiency)Symptoms: Symmetric loss. Starts w/ sensory loss in distal foot & leg. Later motor loss in lower leg.
Cause: Damage in splenium (posterior part of corpus callosum) causing a disconnection between visual & language systemSymptoms: Patient's can't read in left visual field b/c visual input can't get to language centers on left side of brain
Cause: Loss of neurons (selective of dopamine, noradrenergic, & cholinergic), most notably in hippocampus, entorhinal cortex, association cortices, basal nucleus of MeynertSymptoms:Histological signs: (1) Neuritic Senile Plauqes: Extracellular deposits containing neuritic & glial processes w/ central core of amyloid beta protein (chromosome 21) due to additional cleavage of beta chain by beta-secretase & gamma-secretase (normally just alpha-secretase) (2) Neurofibrillary tangles: Intracellular paired helical fragments due to hyperphosphorylated Tau proteins (stabalize MAPs) that occurs during neuron degeneration (3) Granulovacular degeneration: Intracellular circular zones of cytoplasm
Inability to form new memories
Loss of old memories
Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease)
Cause: LMN (weakening & later destruction) with damage to parts of pyramidal tract & precentral gyrus laterSymptoms: Begins asLMN syndromein one or both hands.LMN syndromeprogresses all other motor neurons (e.g. arms, legs, bulbar motor nuclei)Prognosis: Death 3-5 years after diagnosis
Androgen Insensitivity Syndrome
Cause: X-linked recessive in which androgen receptor for testosterone is defectiveSymptoms: If XY testes develop but don't descend b/c testosterone produced has no effect. Normal female external genitalia, primary amenorrhea, sparse to absent development of pubic or axillary hair, female breasts & body shape, have female sexual identity
Anterior spinal artery syndrome
Cause: Blockage of anterior spinal artery. Resutls in lesioning of LMN in anterior horn (corticospinal tracts) & ALS.Symptoms:UMN syndrome, Loss of pain & temp, Urine retention, Sexual function impaired
Cause: May accompany ahemiplagiaSymptoms: Slow writhing abnormal movements of limbs, trunk, head, face, or tongue
Cause: Lesion of dorsal nerve roots of sacral segmentsSymptoms: Fullness sensation of bladder lost, incontinence, dribbline, no mictrition reflex
Cause: Transection of spinal cord w/ reovery of reflexes in sacral segmentsSymptoms: Bladder fills to threshold pressure & spontaneous reflex leads to emptying
Cause: Lesion of the subthalamic nucleus (so symptoms usually unilateral→hemiballismus). Dopamine receptor agonists can also cause ballismus due to overactivity of direct & underactivity of indirect pathways.Symptoms: Rapid, exaggerated, flinging, or abnormal rotation of limb on side contralateral to the lesion
Cause: Bilateral MLF lesionSymptoms: Inability to adduct either eye upon horizontal gaze (convergence intact b/c center responsible for that is usually intact)
Cause: Likely polygenetic with a psychodynamic aspectSymptoms: Severe cyclic mood changes (severe highs followed by lows). If maniac periods aren't treated in time they may develop into psychosis.Brain activity: Area in prefrontal cortex below genu in corpus callosum has reduced activity during depressive phase & increased during manic phase.Treatment: Mood stabalizers, pyschotherapy, antidepressants
Same asFacial palsy.
Characterized by: Not responsive to stimuli, No spontaneous respiration, pupils dilated & unreactive to light, No vestibulo-ocular reflex, No corneal reflex, Isoelectric EEG
Cause: Lesion of Broca's area [44-pars opercularis, 45-pars triangularis]Symptoms: Speech & writing are difficult with missed syllables. Repetition & naming are abnormal but better than spontaneous speech. Comprehension is only slightly affected.
Brown Sequard Syndrome
Cause: Hemisection of spinal cordSymptoms: IpsilateralLMN syndrome@ level of lesion &UMN syndromebelow level of lesion. Contralateral loss of pain & temp. Ipsilateral loss of touch, vibration, & propioreception.
Carpal Tunnel Syndrome
Cause: Compression of median nerve in carpal tunnel (tendon of flexor pollicis longus, flexor digitorume longus & brevis)Symptoms: Pain or tingnling sensation in hands radiating up arm, Weakness & wasting of innervated muscles,Population: Women more likely
Symptoms: Partial or complete sleep paralysis of skeletal muscle (flaccid w/ areflexia) @ start or end of sleep. Awareness preserved. Most last few seconds.Population: Common in narcolepsy. Mostly in children.
Central medullary syndrome
Cause: Usually pathological cyst that usually develops ventrally & usually in the cervical cord that increases pressure on vetral horns & the anterior white commisureSymptoms:LMN syndrome& loss of pain & temp at level of cyst, stiffness, headaches, & possibley ANS disfunction
Cerebellar lesions (alcohol)
Cause: Loss of neurons (particullarly Purkinje cells) in cerebellar cortex of anterior lobe of & some parts of vermis & gliosis, most likely due to malnutritionSymptoms: Dysmetria of legs, truncal ataxia, lurching gait, intention tremor of trung & legs (NOT arms). Nystagmus, dysarthria, & hypotonia NOT common.Treatment: Alcohol abstinence, improved nutrition. There is improvement but recovery is incomplete.
Cerebellar lesions (cerebro- cerebellum)
Cause: Lesion of cerebro cerebellum (plans & times movement, important in learning sequents movements [e.g. piano])Symptoms: Ipsilateral hypotonia, dysdiadochokinesia, rebound phenomenon, dysmetria, intention tremor. Ataxia, decomposition of movement, dysarthria.
Cerebellar lesions (spino- cerebellum)
Cause: Lesion of spino cerebellum (organizes posture & limb movement)Symptoms: Imbalance (fall to side of lesion), Gait ataxia, Arm ataxia
Cerebellar lesions (vestibulo-cerebellum)
Cause: Lesion of vestibulo cerebellum (balance, head & eye movement organization)Symptoms: Truncal ataxia, wide based stance, can't walk heel-to-toe, Nystagmus, Titubation (head nodding), Head tilt.
Cause: Usually one sided so symptoms occur on ipsilateral side of lesionSymptoms: Limb & truncal ataxia, dysarthria, intention tremor, limb dysmetria, dysdiadochokinesia, rebound phenomenon.Other symptoms (due to damage in region of infarct): Ipsilateral facial weakness & sensory loss.
Cerebellar Tumor (midline)
Cause: Tumor (astrocytoma) in cerebellar midlineSymptoms: Increased ICP (headache, vomiting, papilledema, hydrocephalus). Wide based stance, truncal ataxia, hypotonia (enequal on two sides). Balance disorder (can't tandem walk-heel to toe). Nystagmus.Population: Most commen in children (occuring in 1st decade)
Characterized by: Deep state of unconsciousness. Person is alive but not able to move or respond to environmental stimuli.Glasgow coma scale: Score 3-15. 90% <=8 are in coma & 50% likely to die in 6-8hr. 9-11 moderate severity. >12 minor.Eye Response: (1) No eye opening (2) Eye opening to pain (3) Eye open to verbal command (4) Eye open spontaneousVerbal Response: (1) No verbal response (2) Incomprehensible sound (3) Inapproriate words (4) Confused (5) OrientedMotor Response: (1) No motor response (2) Extension to pain (3) Flexion to pain (4) Withdrawal from pain (5) Localizing pain (6) Obeys commands
Complex Regional Pain Syndrome (CRPS)
Cause: Injury resulting persistent pain even after healing either by persistent sypathetic activity or sensitization of noiceptors to norepinephrineSymptoms: Persistent pain, increased sweating
Cause: Damage to arcuate fasciculus (connects Wernicke's  & Broca's areas [44, 45]).Symptoms: Patient can understand what is said but can't repeat it. When the patient is talking they will recognize mistakes but in their attempts to correct them will only make more.
Corticobulbar fiber damage
Cause: E.g. Posterior limb of internal capsule infaractionSymptoms: Contralateral tongue deviation, Deviation of eyes towards side of lesion, Contralateral lower facial muscle paralysis (patient is still able to wrinkle forhead on both sides)
Cause: Prion disease resulting in spongiform appearance of cortex
Cause: Lesion below the red nucleus (rostral midbrain)Symptoms: Painful stimulus results in extension of arms & legs
Cause: Lesion above the red nucleus (rostral midbrain)Symptoms: Painful stimulus results in flexion of arms & extension of legs
Cause: Repetitive head trauma
Diabetes Insipidus (central)
Cause: Lesion of supraoptic or paraventricular nuclei (e.g. head injury) resulting in reduced ADH secretionSymptoms: Excessive thrist, large urine volume
Cause: Insulin deficiency causes hyperglycemia, which can cause peripheral neuropathiesSymptoms: Sensory (pain & temp) loss (usually symmetric & begins in legs b/c small unmyelinated DRG cells vulnerable to hyperglycemia), Motor disfunction (usually asymmetric), ANS neuropathy.
Drug-induced Dyskinesia (Chorea)
Cause: Side effect of L-Dopa, Some anticonvulsangs or antispychotic drugs, which ehance dopaminergic transmission in basal gangliaSymptoms: Ususally choreic movement, Sometimes dysonias (e.g. facial grimacing or eye closure)
Cause: Drugs that block dopamine receptors or dopamine release.Symptoms: Parkinson's disease like sypmtoms that resolve after withdrawal of the drugs
Cause: Can be inherent or aquired (damage to left lobe). Have smaller cells in magnocellular layers of lateral geniculate nucleus (depth & motion)NEUROSCIENCE: Diseases Symptoms: Problems with print to sound translation, tendency to read words backword, inability to process transient sensory input quickly
Symptoms:Less severe when compared to major depression. Non-disabling long-term symptoms that result in the patient not function or feeling well.
Symptoms: Muscle spasm or sustained posture that are usually segmental resulting in hypertrophy
Emotions (Frontal lobe damage)
Symptoms: Indulgence, Irreverence, Impatient
Emotions (Temporal lobe damage)
Symptoms: Taming, Flattening of emotion, Increased sexual behavior, Loss of some learned fear response
Primary: No clear cause, no aura, no focal symptomsSecondary: Seizure originates from a focal group: (1) Partial-no consciousness alteration (2) Secondary generalized-consciousness alteration (3) Primary generalized. There is usually an aura preceding onset of parial seizures.Treatment: Reduce Na+ channels [Phenytoin,carbamazepine], Enhance GABA [benzodiazapine,barbituates]
Cause: Seizures originating in temporal lobeSymptoms: Olfactory or gustatory hallucinations, followed by mood change, & lapse into dreamy state. Finally a motor phase. After recovery patients can't recall the experince.
Cause: Lesion of corticobulbar tract, facial nuclues, or facial nerveSymptoms: (1) Corticobulbar tract: Contralateral lower face paralysis (2)
Fatal familial insomnia
Cause: Prion disease. Selective atrophy of some thalamic nuclei, malfunction of ANS (↑Sympathetics).Symptoms: Progressive untreatable insomnia. Also has motor signs, memory & attention deficit.
Cause: Spincerebellar degradationSymptoms: Onset in 1st or 2nd decade. Progressive limb & gait ataxia. Absent deep tendon reflexes & sensory axonal neuropathy.Histological signs: Atrophy of dorsal columns, corticospinal tracts, & spinocerebellar tracts
Cause: Ventromedial hypothalamic syndrome due to damageSymptoms: Disorder of caloric balance charaterized by obesity (besides other symptoms)
Cause: Lesion of angular gyrus (Area 39), which translates visual patters into meaningful informationSymptoms: Reading & writing very abnormal while Naming is often abnormal
Symptoms: Can't produce or understand language in any form
Grand Mal Seizure
Symptoms: A primary generalized seizure (1) Tonic phase-30s (2) Clonic phase-1-2min jerking (3) Postictal phase-sleepy disoriented, headache, muscle soreness,
Cause: Autoimmune disorder following viral respiratory or GI infections resulting in demylenation of PNSSymptoms: Progressive muscle weakness & paralysis. Usually have good recovery.Population: Males more commonDiagnosis: Protein in CSF (100-300mg/dL), NCV (nerve conduction velocity), EMG (electromyography), Plasma exchangeTreatment: Immune globulin
Symptoms: Gait in which one arm held flexed & ipsilateral leg is extended so arm does not swing & leg is swung around to clear ground. May have athetosis.
Cause: Reduced motility in distal colon due to parasympathetic dysfunctionSymptoms: Feces gets trapped causing abnormal dilation (megacolon)
Cause: Reduced ipsiliataral sympathetic activity (1) Lesion of hyothalamospinal pathway (2) Compession of sympathetic chain [e.g. apical lung tumor] (3) Postganglion lesion [e.g. tumor in cavernous sinus]Symptoms: Ipsilateral miosis, ptosis, ahydrosis
Cause: Bilateral degeneration of striatal neurons with D2 receptors resulting in underactivity of indirect pathway due to excessive # of CAG repeats on chromosme 4 (autosomal dominant)Symptoms: Bilateral dyskinesia, involuntary movement of head, arms, & legs, hypotonia, depressionHistological signs: Striatel atrophy w/ preferential loss of spiny neurons w/ D2 receptors. There is also a reduction in GABA & glutamate decarboxylase.Treatment: (1) Antidepressants to manage depression associated w/ HD. (2) Haloperidol [D2 anatgonist] will increase indirect pathway activity but may lead to difficulty swallowing, speaking, and walking.
Cause: Lesion of anterior hypothalamusSymptoms: Increase in metabolism, shivering, peripheral vasoconstriction (reduce heat loss)
Symptoms: Pre-sleep dreams.Population: Common innarcolepsy.
Cause: Lesion of posterior hypothalamusSymptoms: Decrease in metabolism & motor activity, peripheral vasodilation (increase heat loss)
Internuclear Ophthalmoplegia (MLF
Cause: Lesion of MLFSymptoms: Inability to adduct eye on ipsilateral side of the lesion during horizontal gaze (convergence maintained)
Cause: Sudden change of light dark cylce different from internal clockSymptoms: Night time insomnia, daytime sleepiness (since clock is slow flights east are harder to recover from)Treatment: 1-3mg melatonin in evening one hour before going to bed
Sames asEmotions (Temporal lobe damage)
Symptoms: Prion disease
Lambert Eaton Syndrome
Cause: Autoimmune (x-linking) Vgated Ca2+ channels in motor neuron terminals (often in small [oat] cell lung cancer)Symptoms: Muscle weakness that improves with activity, Reflexes usually decreasedTreatment:4-aminopyridine,Calcium gluconate, Plasma exchange, Tumor removal
Cause: Lead in system via lungs, skin, or gutSymptoms (adult): Focal weakness of extensors of fingers, wrist & arms. Bilateral arm weakness & wasting in chronic cases. Virtually no sensory symptoms. Memory & concentration problems.Symptoms (children <6yo): Encephalopathy, Reduced IQ, ADD, Learning disability. High levels can cause mental retardation, como, or death.Symptoms (infants): Encephalopathy
Leprocy (Hansen's Disease)
Cause: Infection w/ mycobacterium leprae preferentially proliferate in interior of unmyelinated axons causing nerve compression & ischemiaSymptoms: Skin lesions, Profound sensory lossTransfer: Prolonged contact w/ infected individual. Enters through skin lesion.
Cause: Any disease process that can damage a LMN (e.g. Amoyotrophic lateral sclerosis, peripheral nerve damage, ect.)Symptoms: Hyporeflexia/areflexia, Flaccid paralysis, Muscle wasting, Fasciculations (sponataneous twitches), Fibrillations (EMG recordings of fasciculations)
Locked in Syndrome
Cause: Usually develops after blockage of basilar artery resulting in enormous pontine infarctionSymtpoms: Complete paralysis of voluntary muslces in all parts of body except for those that control verticle eye movements (mesencephalic reticular formation in midbrain organizes verticle eye movements), Fully aware & able to think
Cause: Autosomal recessive disorder on chromosome 11 that causes massive loss of Purkinje cells in cerebellar cortexSymptoms (motor): Ataxia at first walking, dysarthria, facial weakness, oculomotor weakness, delayed motor developmentSymptoms (other): Growth & sexual development retardation, Immune deficiency, Death within 3 decades
Symptoms: Inability to work, focus, eat, sleep, & enjoy pleasurable activities
Cause: Reduced blood flow to anteromediallateral pons due to (1) Short circumferential branches of basilar arterySymptoms: (1) Hemiataxia (ipsilateral) (2) Heimplegia (contralateral) (3) Hemianesthesia of face (ipsilateral) (4) Hemiplegia of muscle of mastication (ipsilateral)
Description: Autoimmune (Type IV Hypersensitivity[delayed type], may be due tomolecular mimicry)Symptoms: Vision loss [CN II only CN affected], Diplopia [Processes affecting conjugate eye movements affected], Muscle weakness [Corticospinal tract], Poor coordination, balance, & speech [Cerebellum], Altered sensation [Lesions in spinal cord]Treatment: Symptoms reduce in colder temperatures due to improved conductionDefect: Oligoclonal expansion ofTh1memory cells against a variety of nerve associated phospholipids/glycolipidsResult: Nerve cell death results in release of MBP (myelin basic protein) & other CNS proteins resulting in antibodies against them, further exacerbating problem through attraction of phagocytes & complement activationDiagnosis: Oligoclonal immunoglobulin in CSF (anti-MBP, etc.)Population: Female:Male (2:1)Susceptibility: Increased with HLA-DR2
Muscular dystrophy (Duchenne)
Cause: X-linked recessive disorder resulting in absence of muscle protein dystrophinSymptoms: Progressive weakness & muscle degeneration. Onset (3-5) years, Inability to walk (10-15) years, Inability to breath 20 years.
Cause: Any disease of the synaptic cleft (e.g. breif nAChR opening times, abnormal ACh to nAChR binding)
Cause: Autoimmune (x-linking) of nAChR channels in NMJ resulting in endocytosis. Sometimes associated w/ tymic tumors.Symptoms: Voluntary muscle weakness that increases w/ activity. Eye muscles often affected first (ptosis, double vision). Swallowing difficulty (frequent chocking), Breathing difficultyTreatment:Neostigmine,Pyridostigmine,Prednisone,Cortisone,Azathioprine,Cyclosporine, Plasma exhange, Thymectomy
Cause: Any defect in transmission of electrical impulses in the muscleNEUROSCIENCE: Diseases
Cause: Autosomal dominant disease where there is reduction of Cl- channels in muscle membrane resulting in slow muscle relaxation b/c Cl- channels are essential in keeping membrane potential near Ecl- during AP recovery when K+ ions are accumulating in transvers tubule systemSymptoms: Increased excitability, K+ accumulation in transverse tubule system can lead to depolarization & spontaneous firing after the end of nerve stimulation, Muscle stiffness, Atrophy
Symptoms: Frequent day-time sleep attacks, REM within 10 minutes of sleep onset,Cataplexy&hypnagogic hallucinationscommon, Day-time sleepiness can causesleep apneawhich can reduce latency to sleep 2min [5min normal].
Symptoms: Usually awakenings from REM w/ detailed recall of dreamPopulation: Mostly in children
Cold: GI flu symptoms, Tachycarida, Hypertension, 2nd & 3rd days are worst, Not longer than 5-7 days, Hyposomnia can continue for weeksWarm:Methadoneused to replace opiates & dose reduced over 3 weeks, High chance of break off, Hypertension, Tachycardia
Cause: Characterized by reducedbenzodiazapinebinding sits in frontal lobe than in normal brains
Cause: Bilateral spinal cord injurySymptoms:LMN syndrome@ level of lesion &UMN syndromebelow. Urine retention. After several months flexor spasms decrease w/ development of stage of paraplegia in flexion. Loss of ALL somatosensory perception below the lesion.
Cause: Degeneration of dopaminergic neurons in SNc. Lesions also in locus ceruleus, raphe nuclei, basal nucleus of Meynert, cerebral cortex, central & peripheral ANS.Symptoms: Resting tremor (5Hz) that is suppressed during voluntary movement, Poor postural reflexes, Rigidity, Stooped posture, Slow shuffling gait, Poor arm swinging, Glabellar reflex, Impaired speech, DementiaStages: (1) Unilateral (2) Bilateral w/ postural reflexes (3) Bliateral w/o postural reflexes (4) Severe disability w/ some movement (5) AkinesiaHistological signs: Absence of neuromelanin in SNc (loss of black pigmentation), Selective loss of some noradrenergic & cholinergic neurons, Lewy bodies (granules containing protein) in degenerating cellsTreatment:L-dopa&Carbidopa(Sinemet),Bromocriptine,Pergolide,Amantadine,Selegiline,Entacapone,Tolcapone,Benztropine. Surgically lesion subthalamic nucleus, Gpi, Thalamus. Deep brain stimulation.
Periodic Limb Movements in Sleep (PLMS)
Symptoms: Periodic movements (30s interval) during NREM.
Persistent vegetative state
Characterized by: Sometimes develops after coma. Lost ability to think & are not aware of environment [no higher brain function] but still able to perform NON-cognitive function. Unable to respond to meaningful environmental stimuli.
Petit Mal Seizure
Symptoms: Absence seizure of children, 10s cessation of all motor activity, loss of consciousness, no postictal period
Pfiesteria piscicida (dinoflagellate) toxin
Symtpoms: Toxin upon skin contact or inhalation causes severe nuerological symptoms including, confusion, disorientation, severe memory loss, & poor concentration
Symptoms: Dementia that is clinically difficult to distinguish from AD at onset. Death within 10 years. Behavioural disturbances & aphasia.Histological signs: (1) Cortical atrophy localized in frontal or temporal lobe (usually unilateral) (2) Astrogliosis w/ many residual neurons containing Pick's bodies composed of densely packed neurofilaments (3) Depletion of cholinergic neurons (particularly in basal nucleus of Meynert)Population: Women are more at risk
Cause: Viral infection that affects mostly motor neurons in ventral hornsSymptoms: Muscle weakenss, in severe cases permanent paralysis & deathTransfer: Contact with infected secretions
Cause: Genetic defect in protein that normally holds the nucleus & cells togetherSymptoms: Acclerated aging evident at about 2 years after birth & children die between 8-21 years of heart disease
REM Behaviour Disorder
Symptoms: Abnormal muscle activity during REM (e.g. chin & arms, NOT legs). Suffer vivid dream enactment.
Restless Legs Syndrome (RLS)
Symptoms: Urge to move legs when sitting or lying delaying sleep onset.
Cause: Likely polygenetic with a psychodynamic aspectSymptoms: Cognitive disfunction, Social/occupational dysfunction, Disorganized speech, Grossly disorganized or catatonic behaviorPrognosis: Generally poor with pateints with negative symptoms (loss of function) having a poorer progonis than those with positive ones (gain of function)Treatment:Haloperidol,Perphenazine,Clozapine,Olazapine
Seasonal Affective Disorder (SAD)
Symptoms: Depression during seasons of reduced light
Types: (1) Obstructive (2) Central: Disruption of respiratory centers in pons (3) Mixed: Central & Obstructive (4) Hypnograms. Mean latency to sleep 3min [5min normal].
Sleep Terrors (parasomnia)
Symptoms: Partial arousals from NREM. Often associated w/sleep walking.Population: Most commen in children.
Sleep walking (parasomnia)
Symptoms: Occurs in first 1-2 hours of sleep. Usually NREM-4.
Slow channel syndrome
Cause: Inherited rare condition that results in prolonged opening of nAChR when ACh binds causing a depolarizing blockSymptoms: Muscle weakness, Rapid fatigue, Progressive atrophy
Symptoms: Dystonia of the neck (e.g. SCM muscle)
Cause: Initial stage of UMN syndrome, resulting in flaccid paralysis (mechanism is not well understood)
Cause: Autoimmune disease that is a significant feature of rheumatic fever causing basal ganglion inflammationSymptoms: Onset between 5-15yo & a few month after infection. Choreic movements may be unilateral & recovery is good for nearly all patients.Population: Female:Male (3:1)
Cause: Some antipsychotic drugs (e.g.Haloperidol,Perphenazine)Symptoms: Commonly stereotypic movements of jaw, lips, & tonguePopulation: Older patients at more risk of disorder even after drugs are discontinued
Symptoms: Sterotyped movements that are usually transient & coordinated
Tongue deviation on protrusion
UMN damage: Deveiation towards contralateral side (e.g. posterior limb of internal capsule infaraction)LMN damage (CN XII): Deviation towards side of lesion
Cause: Autosomal dominant diseaseSymptoms: Onset @ 7yo. Multifocal tics & may have hyperactivity disorderPopulation: Female:Male (1:9)
Transcortical motor aphasia
Cause: Lesion in cortex superior to Broca's area (44 & 45)Symptoms: Same as Broca's aphasia but less severe & repitition is preserved. Usually much better at naming compared with spontaneous speech.
Transcortical sensory aphasia
Cause: Lesion in secondary association cortex (perisylvian area)Symptoms: Fluent speech w/ impaired comprehension, Naming proglems, Normal repetition, Semantic retrieval deficit, Normal syntax and phonetics. Inability to speak spontaneously.
Transient global amnesia
Cause: TIA, many othersSymptoms: Brief phase of retrograde amnesia associated w/ a sudden anterograde amnesia lasting minutes to days.
Cause: Damage to motor cortex or axonsSymptoms: Initial period of flaccidity (spinal shock). Followed by hyperreflexia, Extensor plantar response (Babiski reflex), No muscle wasting, Urine retention, Sexual disfunction. Symptoms are ipsilateral if below pyramidal dessucation (in medulla) & contralateral if above.
Cause: Reduced blood flow to posterolateral medulla due to (1) Posterior Inferior Cerebellar Artery (PICA) occlusion (2) Vertebral Artery occlusionSymptoms: (1) Difficulties swallowing, hoarseness (2) Dizziness, nausea & vomiting (3) Nystagmus, problems w/ balance & gait (4) Loss of pain & temp on one side of face & opposite side of body (5) Uncontrollable hiccups (sometimes)
Cause: Reduced blood flow to anteromedial midbrain due to occlusion of short penetrating branches off of (1) Basilar artery (2) Posterior communicating arterySymptoms: (1) Parkinsonism (contralateral) (2) Hemiplegia (contralateral) (3) Facial & hypoglossal paralysis (contralateral) (4) Oculomotor paralysis w/ wide fixed pupils (ipsilateral)
Cause: Damage to posterior section of left auditory cortex (Area 22-Wernicke's area)Symptoms: Speech is fluent but nonsensical. Repetition abnormal. Poor comprehension (reading better than writing). Good penmenship but misspelling & inaccuracies. Wrong names.