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Neuro pt II Flashcards

1
Q

Drug Induced parkinsonism

A
  • D2 receptor antagonists (Phenothiazines, treatment of psychosis)
  • Drugs that deplete dopamine stores within nerve endings (ie reserpine)
  • Metabolite of MPTP (synthetic narcotic), damages nigral SN mitochondria
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2
Q

Vascular parkinsonism

A

Strokes affecting circuits in basal ganglia - ie, lose regulation

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3
Q

Chronic traumatic encephalopathy

A

Damage to cerebral blood vessels and other structures ie nigral cells, interactions with midbrain, during violent head movements with excessive cranial acceleration - ie mohammed ali

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4
Q

Encephalitis Lethargica (Viral infection)

A

Degeneration of SNc

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5
Q

Huntington’s chorea

A

Genetic hyperkinetic disorder of Basal Ganglia - Loss of spiny neurons at the beginning of the INDIRECT pathway. ie loss of D2R expression. So decreased inhibition to the thalamus, leading to dance like movements.
Other choreas incl sydenham chorea, drug-induced chorea (L-dopa), and athetosis.

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6
Q

hemiballismus

A

Stroke related hyperkinetic disorder of basal ganglia
Commonly an infarct of STN. Often unilateral, with contralateral manifestation. No longer able to send its positive output to GPi /SNr and thus less inhibition of the thalamus, less inhibition of movement - ballistic movements ie sudden, rapid, flinging, rotational mvmts

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7
Q

Bromocriptine

A

D2 agonist

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8
Q

Pergolide

A

D1 and D2 agonist

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9
Q

Amantadine

A

Increases release of dopamine from surviving Substantia Nigra compacta cells ie treat parkinsons

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10
Q

Selegline (deprenyl)

A

Blocks breakdown of dopamine (MAOi). Treatment of parkinsons

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11
Q

Entacapone and Tolacpone

A

Inhibitors of COMT, block bdown of dopamine - parkinsons treatment

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12
Q

Benzotropine

A

Anticholinergic, muscarinic antagonist. PD treatment, cholinergic projections from substantia nigra to striatal medium of inhibitory path, so decreasing this path.

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13
Q

Surgical therapies for parkinsons

A

Stereotaxic lesions of subthalamic nuc - reduces excitatory input to GPi - ballismus undesirable prospect
GPi (pallidus internus) lesion - reduces inhibitory input to thalamus directly. Disinhibited thalamus free to restore cortical excitation and reverse hypokinesia

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14
Q

Treatments for huntingtons

A

Most common is symptomatic - antidepressants
Drugs to limit chorea: antagonists of D2 receptors (activating indirect path), VMAT inhibitors (reduce mvmt of dopamine into vesicles, deminishing exocytosis, reduced dopamine levels, reduced dopamine may dishiibit surviving straitopallidal cells in indirect path)

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15
Q

Alpha Iatrotoxin

A

Ie black widow. Massive increase of ACh release, tetany.

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16
Q

Lambert-Eaton

A

Autoimmune antibodies against VG Ca channels
Often in bronchial (oat cell) carcinoma
EPP reduced, not reach stimulus. Reduced reflexes, Muscle weakness - can be improved with activity - ie maintain Ca channel opening
Treat: remove tumour, immunosuppresants, plasma exchang, calcium gluconate can enhance Ca influx, 4-aminopyridine prolongs presynaptic AP

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17
Q

AChEsterase Deficiency

A

Congenital myasthenia. Accumulation of ACh. EPP amplitude increased and prolonged. Only single mscl nerve stimulation at long intervals produces a single twitch. Repetitive causes EPP temporal summation, –> depolarization block, and reduced muscle twitch

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18
Q

Slow channel syndrome

A

Congenital myasthenia - ACh binding to nicotinic ACh receptors (nAChR), causes prolonged opening of channels. Prolonged depol, EPP. –> Depolarizatino block, decr muscle twitch.

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19
Q

FOrms of congenital myasthenias

A

AChEsterase deficiency –> depolarization block
Slow channel syndrome –> prolonged opening, depol block
Fast channel syndrome - close quickly, small EPPs, not reaching threshold
Abnormal binding of ACh to nAChR

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20
Q

Myasthenia Gravis

A

Antibodies to nAChR. -
Cause cross linking and thus internalization and degradation of nAChR.
Endplat chngs: decreased jnxnl folds, reduced depth, reduced Na channels, less AChR, larger synaptic cleft.
Weakness of voluntary muscles, esp eyes (worked a lot through day, diplopia)
Chronic fatigue, serum from patients can cause disease in animals..
WANING pattern of EMG recordings during rpetitive stimulation

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21
Q

EMG differences MG and LE

A

In LE (lambert eaton) see a waxing pattern - depolarization is maintained longer, so prolonged opening of Ca channels.

In MG- see a waning pattern, small EPPs not able to invoke AP

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22
Q

Tensilon Test

A

Injection of edrophonium (AChE inhibitor), muscular strength temporary recovers -diagnostic of myasthenia gravis.

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23
Q

Treatment for Myasthenia gravis

A

Plasma xchng - temp relef
Immunosuppressants - azathioprine, corticosteroids
Pyridogstigmine (AChE inhibt) in conjuction with propanthline (pyrido is a global AChe ie musc and nic, so propanthaline decreases some side effects).
Thymectomy

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24
Q

Myotonia Congenita

A

AD - less chloride channelsin muscle membrane. Normally - keep potential close to Ecl during recovery of AP whil K is accumulating in TTS (transverse tubular systm).
Causes increased excitability (closer to threshold) - spontaneous firing after stimulation ceased
–> muscle stiffness and hypertrophy

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25
Q

Decorticate posture

A

Cerebral lesion (above red nucleus) affecting corticospinal and corticobulbar systms.
Red nucleus –> increases flexion in upper limbs
Pontine and medullary motor centers - promote extension of the legs
Can be elicited by noxious stimuli if not expressed tonically.

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26
Q

Decerebrate posture

A

Muscle tone of arms favors extension (loss of red nucleus).

Remaining brainstem motor centres contiue promoting leg extension.

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27
Q

Station

A

Sensitive to damage to conscious and unconscious sensory systems and the motor systems. Ability to stand steadily with feet together - may deteriorate when eyes are closed due to lack of visual compensation.

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28
Q

Intention tremor

A

Becomes apparent with purposeful movement, and amplitude tends to increase as target is approached. Cerebellar dysfunction is causal

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29
Q

Parkinson’s disease clinical manifestations

A

Hyposmia - degen of olfac bulbs. Autonomic dysfunction - erectile, cardiac, GI
REM sleep disorder - breakthrough of muscular rigor (pontine degeneration)
Above are all prodromal
Akinesia/bradykinesia, initiation of mvmt difficult
Facial masking - expression diminishes
Rigidity - revealed during assessment of passive mvmt. - Cogwheel rigidity, lead pipe rigidity.
Loss of postural reflexes - patints fall easily if station is disrupted
Shuffling gait, turning difficult, small steps replace pivoting. Festination - unintntional accelration, Gait may normalize with sensory cues
Loss of habituation to glabellar stimulation
Quiet, hoarse, monotonous speech with accelerative bursts (festination)

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30
Q

Stages of Parkinson Disease

A
  1. Unilateral
  2. Bilateral with preserved postural reflexes
  3. Bilateral with loss of postural reflexes
  4. Severe disability with some movement
  5. Akinesia
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31
Q

Athetosis

A

Writhing movements - tied to BG disease ie athetoid cerebral palsy. Striatal or thalamic injury. Can overlap with choreatic mvmts, or can accompany hemiplegia.

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32
Q

Hungtington’s Presentations

A

AD, young adults
May first present emotional dysregulation (disinhibition, impulsivity, emotional lability)
Facial/oral musculature - grimacing, eyebrow raising, lingual protrustion
Piano playing postur
Progression - life expectancy two post diagnostic decades

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33
Q

Sydenham’s Chorea

A

After rheumatic fever, choreatic mvmts emerge (autoimmune) somtimes unilatrally
Aget onset typically 5-15 yrs
Motor manifestations rel to basal gangliar inflammation
Recovery: 6 wks

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34
Q

Deep brain stimulation on parkinson’s

A

Thalamic stimulation - directly increase excitatory output to cortex
Paradoxical effects of stim of GPi - maybe activation of local inhibitory neurons?
Subthalamic stimulation - mysterious effects

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35
Q

Spino-cerebellum

A

Overlaps with anterior lobe of cerebellum (above primary fissue). Spinal cord provides this region with sensory feedback regarding consequences of motor activity. Assisting regulation of gross truncal and limb movemtns.

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36
Q

Superior cerebellar peduncles

A

Cerebellar signals to pons and midbrain (except those destined for vestibular nuclei)

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37
Q

Inferior cerebellar peduncles

A

Relay information from spinal levels into the cerebellum, also contributes communications with the olive, CN VIII, vestibular nuclei

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38
Q

Middle cerebellar peduncles

A

Information from pons to cerebellum

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39
Q

Lesion of vestibulocerebellum

A

Equilibrium disturbances - nystagmus (ocular ataxia), tilted head, titubation (head nodding), truncal ataxia (imbalance) with compensatory wide based stance - impaired tandem wakling

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40
Q

Lesion of spino-cerebellum

A

Disturbances affect posture and movement of limbs - ataxias of the limbs common (ipsi)
Gait ataxia accompanied by lurching to the side of the lesion

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41
Q

Lesion of cerebro-cerebellum

A

Affect accuracy and timing of movement. Ataxia (also distal), decomposition of mvmt, dysarthria, dyssynergia (uncoordination of limbs) - dysdiadokinesia (inab to perf rapidly alt mvmts), dysmetria (past-pointing)
Hypotonia, intention tremor, rebound phenomenon

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42
Q

Cerebellar tumour (ie astrocytoma) in midline region

A

Wide based stance, truncal ataxia, disorder of balance (no heel to toe), nystagmus

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43
Q

Cerebellar stroke (usually one-sided)

A

IPSI limb ataxia, intention tremor, dysarthria, dysdiachokinesia tc

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44
Q

Thiamine deficiency malnutrtion through alcohol abuse effect on cerebellum

A

Damages anterior lobe of cerebellum. Dysmetria of legs but not arms. Ataxic stance and gait, intention tremor of legs but not arms

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45
Q

Louis Bar syndrome

A

(chrom 11) damages cerebellar cortex - massive loss of purkinje cells. Ataxia at first walking, dysarthria, facial and ocular weakness, sensitivity to ionizing radioation, increased vulnerability to cancers, skin and eyes - small dilated blood vessels

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46
Q

Cerebellar Cognitive affective syndrome

A

Lesions of posterior lobe are considered to correlate with dysfunctional cognitive and emotional systems, lead to emotional blunting and depression, disinhibition and psychosis. Executive, visual-spatial and linguistic deterioration, - dysmetria of thought.

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47
Q

Tropical Spastic Paraparesis (TSP)

A

(HAM HTLV-1 assoc myelopathy) Degenerative neuro disease - demyelination of the spinal cord. Hyperreflexia, spasticity, weakness of LL and gait abnormality.
Virus, spread via placenta, blood, etc.
Diag. via blood test, MRI, nerve conduction studies EMB
Treat with corticosteroids

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48
Q

Conduction velocity change if motorneuron soma injurty (axon intact)

A

little or no reduction in motor, no change in sensory CV

49
Q

Peripheral nerve changes in CV with compression, demyelination, axonal degeneration mild and severe

A

Compression: slowing of motor and sensory at site
Demyelination: marked slowing of motor and sensory
Axonal degen mild: slight reduction of motor and sensory
Axonal degen severe - NO conduction of motor or sensory

NO changes if NMJ or at muscle

50
Q

Leprosy (Hansen’s disease)

A

Mycobacterium lepra. Access body via skin lesions, multiplies on axons and ISF.
Profound sensory loss, particularly PAIN and T (because small neurons lost first)
Antibiotics: dopsine, rifampin, cloazimine

51
Q

Guillan Barre

A

2: 100, 000.
more common in males?
Following viral resp. or GI illness - autoimmune, molecular mimicry.
Demyelination caused by nerve inflammation - slowing or conduction block.
Treat: plasma exchange, immunoglobulin.
Increased protein in CSF, mononuclear count less than 10.
ASCENDING paralysis

52
Q

Lead poisoning/plumbism

A

Motor deficiencies mainly ,virtually nO sensory loss.
Focal weakness of extensor muscles or fingers, wrists, arms. Bilatearl arm weakness and wasting chronically.
Motor neuropathy in adults, encephalopathy in children less than 6 yrs.

53
Q

Alcoholic Peripheral Neuropathy

A

> 80-100g of alcohol/day for >10 yrs. Malnutrition leads to vitamin B1 deficiency - motor and sensory losses SYMMETRICALLY.
Sensory neuropahty FIRST, DISTAL to proximal.
Motor neuropathy SECOND, typically in lower leg

54
Q

Diabetic neuropathy

A

Poorly controlled diabetes. Functional: sesory (usually symmetric), motor (usually Asymmetric), autonomic neuropathy

Sensory - begins distal legs, stocking distribution
Losses by abnormalities of unmyelinated axons carrying P and T

Sensory endings and axons of SMALL unmyelinated DRG cells - vulnerable to hyperglycemia. Failure of cell body to supply distant parts with nutrients.

55
Q

Vegetative State “awake coma”

A

Damage to hippocampal formation and cerebral cortex (hypoxia)
Develops after coma
Lose ability to think, speak, and respond and are not aware of enviro.
Perform non-cog functions and NORMAL sleep patterns

56
Q

Brain death

A 
Not responsive to speech, pain, or other stimuli
No spontaneous respiration
Pupils dilated, not reactive to light
no VOR
No corneal reflex
Isoelectric EEG
57
Q

Locked-in syndrome

A

Injury to LOWER brain stem
Tetraplegia, ho horizontal eye movements, , vegetative dysregulation
Typically infarct of basilar artery - can think but can’t communicate except for vertical eye mvmt and blinking

58
Q

Causes of coma

A

Lesions in mesencephalon - paramedian reticular formation
Lesion of posterior lateal hypothalamus
Thalamus lesion
Bilateral impairment to both hemispheres (trauma, metabolic)
Supratentorial mass lesions - epi sub etc.
Subtentorial (infratentorial lesions) ie brain stem etc cerebellar
Metabolic and diffuse cerebral

59
Q

Glasgow Coma Scale (GCS)

A 
Eyes - 4
Motor - 6
Verbal - 5
Critical score is 8
Severe head injury <8, moderate head injury 8-12, mild 12-15.
60
Q

Types of coma

A

Coma without focal signs or meningism (most common),
Coma without focal signs with meningism
Coma with focal signs

61
Q

Possible cause of small, reactive pupils (coma eval)

A

Diencephalic, or diffuse effects of rugs, metabolic encephalopathy etc

62
Q

CN III (Uncal herniation) effect on pupils

A

Unilateral, dilated fixed pupil

63
Q

Effect of pretctal lesion on pupils (coma eval)

A

large, fixed

64
Q

Effect of midbrain lesion on pupils

A

Midposition, fixed

65
Q

POntine lesion on pupils

A

pinpoint

66
Q

Tropical Spastic Paraparesis (TSP)

A

Chronic degenerative neuro disease, demyelination of spinal cord. Hyperreflexia, spasticity, weakness of lower limbs and gait abnormality.
HTLV-1 Associated myelopathy - spread thru placenta, bld transfusion, breastfeeding, needles, sex

HAM/TSP in tropical locales - adults btwn 30-40, more common in F.
Can remain undetected, when immune system’s response to virus causes diffuse (rather than patchy) demyelination, legs gradually lose strength and flexibility.

Diagnose: blood tests, MRI of spinal cord, nerve conduction studies, EMG
Neuro eam: Knee jerk and ankle bilateral v brisk, bilateral babinski, muscle tone in legs bilaterally elevated
Treatment: corticosteroids
Differentials: HIV and MS related myelopathy.- sensitive to confection with HIV

67
Q

Repeat expansion location and mechanisms

A
  1. Protein coding region - gain of function, or toxic protein
  2. RNA coding regions ie introns and UTRs - mRNA instability, translation effects
  3. Non-coding regions - transcriptional effects, interference with regulation of nearby genes.
68
Q

Slippage - mechanism for triplet repeat expansion

A

DNA pol - replicated repeated DNA sequence. Is arrested and dissociates from newly synth strand - newly synth strand separates, bubble - should base pair back down but forms a loop and realigns with a different repeate. DNA pol reminds and replication resumes - but have a longer daughter strand. Stutter, mechanism for EXPANSION only.

69
Q

Unequal crossing over

A

Mechanism for triplet repeat expansion or contraction.
During meisois, two pairs of sister chromatids line up. Repetitive sequences, one region of chromatid does not line up exactly with its corresponding repetitive region in other chromatids – two germ cells, one shortened repetitive region and one with an expanded one.

70
Q

Anticipation

A

Characteristic of triplet repeat disorders. Increase in severity and decrease in age of onset in successive generations of a disease. Due to repeat expansion through generations.

71
Q

Threshold numbers for Huntington’s (AD), Fragile X (x linked), and myotonic dystrophy (AD)

A

HD: CAG, normal 9-35, pathogenic 36-100
Fragil X: CGG, normal 10-50, pathogenic 200-2000
MD: CTG, normal 5-25, pathogenic 75-11,000

Numbers between normal and pathogenic - premutational, sometimes have mild, late onset phenotype.

72
Q

Huntington’s Disease

A

I: 3-7/100,000, AD, paternal anticipation, polyglutamine disease, CAG repeats within exon 1 - paternal origin - primarily during male gametogenesis.
Two hypotheses: 1. Increase polyglu tract length – protein aggregates, forms inclusion bodies, behaves as a toxin
2. Abnormal protein interacts with TFs and causes dysregulation of gene expresssion
Progressive dementia and involuntary movement. No cure or treatment. Course 15 years from onset, mean onset age 40 years.
Degeneration of neurons in the cerebral cortex, chorea caused by degeneration of basal ganglia. Cognitive and language decline
Positional cloning used to localize-

73
Q

Meiotic drive

A

Germ cells/gametes that contain expanded repeats have a selective advantage. In male - cells with mutation go through cell cycle quicker, more mitoses than without huntington mutation - expand more, then are over-represented int he testes. So when recombination during meiosis, those win.

74
Q

Fragile X syndrome

A

CGG repeat on X chromosome, FMR1 gene has CGG at 5’UTR - allows more methylation of the gene (expanding CpG islands) - FMR1 expression silenced, FMRP protein deficiency - normally involved in RISC complex miRNA function
Mental retardation, learning difficulties, prominent ears, elongated face, macro-ochordism (enlarged testis)
only 50% of affected females manifest learning difficulties
Anticipation in successive gens, (repeat expansion during oogenesis, more sever when female transmits), X chrom mother demonstrates premutation - anticipation expands to give son disease.
Southern blot - indicates number
X chromosomes show breakage in a folate deficient medium - cytogenetic test. Fragile site only in individuals with ful mutation.

75
Q

Myotonic Dystrophy

A

1/8000, multi-systemic, no cure or treatment. AD, maternal anticipation (variable age of onset)
Muscle wasting, esp distal. Cataracts, heart effects, endocrine changes (insulin R), Developmental delay and learning problems. Speech and language.
DM1: most common, myotonia and weakness distal muscle, face and jaw muscle, drooping eyelids
3’UTR CTG repeat of protein kinase gene (DMPK) - sequester and causes abnormal expression of various RNA binding proteins. - altered cell function and widespread splicing alterations
DM2; muscle pain, stiffness fatigue. Weakness in proximal lower extremities ie neck, shoulders, hips, upper legs

76
Q

Friedrich’s Ataxia

A

1/50,000 (carrier 1/110). AR, possible paternal anticipation.
Progressive, neuro-degenerative. Limited pharm treatment, surgical int for spinal and heart problems.
Ataxia and muscle weakness, vision and hearing, scoliosis, diabetes, heart disorders
5-15 yrs, first symptoms difficulty walking, loss of tendon reflexes ankle and knees. Later slurring of speech, vision, and hearing loss. Heart disease most common cause of death. –> wheelchair 10 to 20 years later’
GAA expansion in INTRON 1 of frataxin gene. - alters chromatin through DNA methylation and histone modification. Heterochromatin formation and repression of frataxin gene.
Frataxin involved in mitochondrial iron metabolism

77
Q

Spinocerebellar Ataxia

A

1-5/100,000. AD, AR, or Xlinked. Multiple types, progressive, neurodegenerative, no cure.
Variable symptoms: lack of muscle cord, hands, eyes, speech cord. Full mental capacity retained.
Variable age and life span, trinuc repeat not sex based, 29 different genes identified.
MOST types: CAG trinucleotide expansion in exons. Polyglutamine disorder, expression of mutant gene.
Spinocerebellar ataxia 8 - unique, CTG expansion in 3’ terminal exon of non-protein coding RNA from SCA8 gene. FUnction is unknown, but epansion alters binding.

78
Q

Korsakoff’s syndrome

A

Chronic alcoholics, thiamine deficiency. bilateral losses of cells in the dorsomedial thalamus and mammillary bodies. Confusion, confabulation, memory impairment. Anterograde amnesia and severe retrograde amnesia. Anterograde probably due to damage to diencephalic structures (thalamus) and hippocampus

79
Q

ECT and amnesia

A

ECT used in clinical depression (severe). ECT across brain to evoke seizure. May cause anterograde and retrograde amnesia. Ie may not remember treatment and have impaired memory of events up to several years prior to treatment. Usuallly not permanent amnesia and lifts after several months.

80
Q

Dinoflagellate Pfiesteria Piscicida

A

Marine species - releases toxins into sea, when in contact with skin or inhaled by humans can cause severe neurological symptoms incl confusion, poor concentration, disorientation, and severe memory loss.

81
Q

Development of language in children

A

5-7 mo : language like sounds
7-8 mo : well formed syllables
1-2 years: first word, understand connection between word and visual acoustic appearance
2 years: rich phrase (children language)
3 years: correct grammar, understand rules

82
Q

Lesion of right hemisphere and language

A

Loss of ability to express emotion. Flat, lifeless, and mechanical speech. Ie people with severe left hemisphere damage and intact right hemisphere who cant speak are still able to sing songs and may even learn new songs.

83
Q

Angular Gyrus

A

Combines sensory input to translate the visual patterns of letters and words into meaningful information (and auditory form)

84
Q

Fluent aphasia

A

Patients have fluent speech, but difficulties in comprehension and repetition.

85
Q

Nonfluent aphasia

A

patients have difficulties in articulation, and production of speech (comprehension usually preserved)

86
Q

Wernicke’s aphasia

A

Damage to posterior sector of left auditory association cortex (BA 22) - NO deficits in articulation. Poor comprehension and POOR repetition. Linguistic errors, neologisms - no words. Semantic paraphrasais, phonemic paraphrasias. Language is fluent but meaningless. Sometimes get hemianopia.

87
Q

Transcortical sensory aphasia -

A

Inability to speak spontaneously, and deficits in comprehension. repetition usually preserved. Lesion of the secondary association cortex - perisylvian area - junction of parietal, temporal and occipital lobes - hypoxia.

Fluent speech, impaired comprehension. Sometimes problems nearing things. Repetition is normal (may correct grammar in sentences they don’t understand). Deficit in semantic retreival; syntactic and phonological abilities are not impaired.

88
Q

Gerstman Syndrome

A

Damage to angular gyrus. Translation of visual patterns of letters and words into meaningful information is impaired.
Normal pronunciation, often normal speech content, repetition OK, comprehension ok of spoken language

Compréhension of written language - v ABNORMAL
Writing - v ABNORMAL
Naming - often abnormal

Slight hemiparesis, trouble calculating, finger agnosia, hemianopia

89
Q

Conduction aphasia

A

Lesion of arcuate fascicules. Both language areas intact. Understand but CANNOT repeat it. Say something wrong, realise mistake, but when attempting to correct keeps making mistakes.

Damage of left superior temporal gyrus and inferior parietal lobbe (BA 39,40), may extend to left primary auditory cortex (41, 42), insula and underlying white matter. See Neglect of the Right visual field.

Rhythm: normal
Content: some wrong words
Repetition: abnormal
Slightly abnormal comprehension f spoken
Normal comprehension of spoken
Writing - occasional errors
Naming  - occasional wrong names
90
Q

Broca’s aphasia

A

Comprehension intact.
Damage to broca’s area (inferior left frontal gyrus, BA 44 and 45). Surrounding frontal fields (6, 8, 9, 10, 46). Underlying white matter, insula and basal ganglia

Dysarthria, stuttering, effortful speech. Content: missed syllables, agrammatical, telegraphic.
Repetition ABNORMAL but better than spontaneous.
Comprehension of spoken: normal
Written comp: not as good as for spoken
Writing: clumsy , agrammatical, misspelling
Naming: better than spontaneous speech

Other: hémiplégie, apraxia

91
Q

Transcortical motor aphasia

A

Damage to left dorsolateral frontal area, anterior and superior broca’s (selection of words, gen of motor commoands) and may be damage to broca’s

Non-fluent language
Can repeat longer sentences
Disconnection of the language areas (initiation and control of speech).

Suffer from same defects as broca’s but usually less severe and repetition is preserved. Often significantly better in naming test compared with their spontaneous speech.

92
Q

GLobal aphasia

A

Cannot produce or comprehend language. Ie combo of broca’s, wernicke, and conduction

Everything is abnormal, plus may see hémiplégie.

93
Q

Alexia

A

Damage to Splenium (posterior part) of corpus callosum
World blindness - inability to read the left visual field. Disconnect between visual and language system - ie info from left visual field to right hemisphere, must be sent back to left hemisphere - alexia results from a disruption of this flow.

94
Q

Theory of dyslexia

A

Deficit in development of hemispheric specialisation. More left-handed people here…
Inability to process transient sensory input quickly - speed/rapid conduction in visual system below average. Dyslectic patients have difficulty processing fast, high contrast, visual stimuli - cells in magnocellular layers of LGN smaller than normal?
Discrepancy betwen intelligence and reading ability.

95
Q

HM Case removal of medial temporal lobe - bilateral removal of complete amygdala, uncus, and most of hippocampus

A

Retained Original IQ, language skills, procedural memory acquiring of new skills, long term memory (declarative and nondeclarative)
BUT LOST ability to process new info from immediate or short term memory into long term memory ie profound anterograde amnesia (short term declarative memory). couldnt remember his neurologist after 50 years of contact

96
Q

Case of NA - lesions of thalamus, medial tmporal lobe (incl hippo), and mammilary bodies

A

Sever anterograde amnesia for declarative memories.

Maintained long term memory but sustained some rtrograde amneisa (2 years)

97
Q

Case of RB

A

Ischemic attack during bypass surgery - anterograde anesia, but retained IQ and cognitive ability.
Bilateral lesions - localized to hippocampus, lost CA1 neurons

98
Q

Wernicke Korsakoff Syndrome

A

Thiamine (B1 deficiency) - increased lateral ventricule size, decreased corpus callosum, decreased neuronal number in thalamus, hippocampus, mammillary bodies
Symptoms: confusion, confabulation, memory loss - BOTH anterograde (hippocampal and thalamic) AND retrograde.

99
Q

Guillan Barre clinical symptoms

A

ASCENDING paralysis - rapid onset weakness in the legs, spreading to upper limbs and face, loss of DTR
History of preceding illnes ~2-4 weeks prior (C. jejuni or respiratory)
Autoimmune attacks on peripheral nerves (ganglioside)
Conduction block ( decreased CNV)
Frequenctly CN VII, III, VI, IX, X, and XII
Ie facial paralysis, nystagmus?, swallowing problems.
Treat: plasma infusion of immunoglobulins and plasmapheresis.
Phase I: first symptoms noted, 1-3 weeks until no further deterioration
Phase 2: plateau, two to several weeks
Phase 3: Recovery, extends over 4-6 months.

100
Q

Décorticate Posturing

A

Lesion above the red nucleus
Tracts impaired:
Corticospinal tract mainly flexion
Corticobulbar tract paralysis of motor CN
Other modulators : corticorubral, corticoreticular

Tracts intact:
Rubrospinal - FLEXION of arms
Medullary Reticulospinal - FLEXION of extremities
Pontine Reticulospinal - EXTENSION of extremities (legs)
Vestibulospinal - EXTENSION of extremities (legs)

101
Q

Decerebrate Posturing

A

Lesion below the red nucleus.
Interrupted: corticospinal (flexion impaire), corticobulbar, rubrospinal (no flexion of arms), corticoreticular, corticorubral

Intact: Medullary reticulospinal tract (flexion of extremities)
Pontine reticulospinal (extension of extremities)
Vestibulospinal (extension of extremities)

102
Q

Tetrabenzine

A

VMAT inhibitor, depletes dopamine - used in treatment of Huntington’s

103
Q

Pathology of Huntington’s Disease

A 
Extensive neuronal death in striatum (caudate nucleus and putamen) 
To a lesser, but significant extent in: 
Cerebral cortex
Hippocampus
Cerebellum (purkinje cells)
Others.
104
Q

Weber’s Syndrome

A

Interpeduncular PCA branches (paramedian branches)

Ventromedial midbrain - CN III exiting fibres IPSI, Corticospinal tract - CONTRA hemiparesis, Corticobulbar - CONTRA lower facial paralysis umn signs ie exag gag etc, Substantial nigra - CONTRA parkinsonism (bradykinesia)

105
Q

Structures affected in Wallenberg’s syndrome

A

Vestibular nucleus (nystagmus, vertigo, veering toward lesion), sympathetic tract (IPSI horner’s), ALS (contra loss of P and T body), spinal trigeminall (IPSI loss of P and T face), nucleus ambiguus (hoarseness, dysphagia - differentiates from lateral pontine), inferior cerebellar peduncle (IPSI ataxia), reticular formation (respiratory center) - singultus ie hiccups.

106
Q

Transient Global Amnesia

A

Can be caused by transient cerebral ischemia. Brief phase of retrograde amnesia associated with sudden anterograde amnesia, lasts minutes to days.

107
Q

Prefrontal neocortical area in memory

A

Concerned with WORKING memory, and about stored information referring to the source, helping relate memories to the time and place at which the stored information was received.

108
Q

LTP post-synaptic changes in CA1 neurons

A

High frequency stimulation (100/s) impulses along CA3 schaffer collaterals to CA1 neurons, produces in increase in synaptic efficiency by insertion of new AMPA receptors for Glu on CA1 dendritic spines, and later an increased in the number of synapses between CA3 and CA1 (new dendritic spine formation)

109
Q

Korasakoff’s syndrome (and memory)

A

Vitamin B 1 deficiency. Bilateral losses of cells in dorsomedial thalamus and mamillary bodies. Confusion, confabulation, and severe memory impairment. Also show anterograde and severe retrograde amnesia. Retrograde probably due to damage to diencephalic structures (thalamus) and hippocampus. Alcoholics also show lesions in the neocortex, cerebellum, and brainstem.

110
Q

ECT and memory loss

A

ECT employed for treatment of clinical depression. May cause anterograde and retrograde emnesia. ,Ie might not remember treatment, and may have impaired memory of events up to several years prior to ECT.- not usually a permanent amnesia and may lift after several months

111
Q

Dinoflagellate Pfiesteria Piscicida

A

Marine species releases toxins into the sea, when in contact with skin or are inhaled can cause severe neurological symptoms incl confusion, poor concentration, disorientation, and severe memory loss

112
Q

Damage to R anterior and posterior hemispheres effect on language

A

R anterior: Wrong intonation, monotonous

R posterior: Difficulty in interpretation, understanding context - ie speaking to boss versus friend

113
Q

Damage to right hemisphere effect on pragmatics

A

Difficulty understanding jokes, sarcasm, metaphors and with construction of a story

114
Q

Processing of an incoming spoken word

A

Auditory signal –> auditory pathways –> Wernicke’s area –> evocation of words meaning in areas NEAR wernicke’s area

115
Q

Outgoing spoken word processing

A

Nonverbal meanings –> conversion to an acoustic image in Wernicke’s area –> arcuate fasciculus –> Broca’s area –> motor cortex

116
Q

Reading processing

A

Input from visual cortices –> Wernicke’s area –> evocation of word’s meaning in areas near Wernicke’s area

117
Q

Writing processing

A

Nonverbal meanings –> conversion to a motor/visual image in Wernicke’s area –> arcuate fasciculus –> Broca’s area –> premotor area above Broca’s area

118
Q

Best motor response components of GCS

A 
6 - obeys
5 - localizes
4 - withdraws
3- abnormal flexion (decorticate)
2 - abnormal extension (decerebrate)
1 - no response
119
Q

Idiopathic normal pressure hydrocephalus in elderly

A

Dementia, Urinary incontinente, and symmetric gait instability.

Neuro (6 decks)

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