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Neurological System > 2-CNS > Flashcards

2-CNS Flashcards

1
Q

Describe cortical dementia. Example diseases? Symptoms?

A

E.g. - alzheimer, CJD

Disorder affecting the cerebral cortex, playing an important role in memory and language.

Signs: Memory Loss, Aphasia, Apraxia, Agnosia

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2
Q

Describe subcortical dementia. Examples? Symptoms?

A

non-alzheimer demetias

Dysfunction in parts of the brain that are beneath the cortex.

Frontostriatal pathways facilitate speed/efficiency of thought.

Signs: Slowed Thinking, Executive Dysfunction

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3
Q

Define the terms Pyramidal and Extrapyramidal.

A

Pyramidal: motor system with fibers originating from the cortex; CST called the pyramid in the medulla

Extrapyramidal: motor system with fibers originating from the basal nuclei and cerebellum

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4
Q

What are the contents of the Basal Nuclei?

A 
Caudate 
Putamen 
Globus Pallidus
Subthalamic Nucleus
Substantia Nigra
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5
Q

Describe the features of parkinson disease.

A

Tremor, Bradykinesia, Cogwheel rigidity, postural instability

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6
Q

Define dementia.

A

An acquired, persistent decline of intellectual functioning. Impaired memory and at least one other cognitive domain (aphasia, apraxia, agnosia, executive function)

No clouding
No underlying psychiatric disease

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7
Q

What is mild cognitive impairment?

A

MCI (ADLs intact)

Memory impairment in people who are not demented

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8
Q

Describe Alzheimer Disease.

A

Most common dementia over 65.

Progressive, degenerative brain disease characterized by memory loss and loss of other cognitive functions

Loss of short term memory prominent early

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9
Q

What are the 3 paths of alzheimer disease?

A

Beta-secretase: protein cleaving enzyme that causes abnormal metabolism and deposition of amyloid protein

Cholinergic deficiency: in cortex and basal forebrain - contributing to cognitive deficits

Glutamate: overstimulation via glutamate NT leading to excitotoxicity and neuronal cell death.

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10
Q

What chromosome is most commonly associated with alzheimer disease?

A

19 - apolipoprotein E4 (ApoE4 gene)

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11
Q

How is alzheimer diagnosed?

A

Via clinical criteria while the patient is still living

Deposition of amyloid-beta protein, neurofibrillary tangles, loss of neurons will be seen on autopsy.

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12
Q

Describe the drugs that can be used to treat alzheimer disease.

A

Cholinesterase inhibitors:
1. Donepezil: Severe cases

  1. Rivastigmine: mild to mod. along with treatment for dementia related to parkinson
  2. Tacrine: mild to mod. must monitor liver ALT levels
  3. Galantamine - mild to mod

NMDA Receptor Antagonists:

  1. Memantine: moderate to severe. Can cause constipation, hypertension, dizziness, headache.
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13
Q

Describe Diffuse Lewy Body Dementia (DLB)

A

(Video in ppt)
Second most common form of dementia.
Starts with parkinsonian symptoms followed by decline.

Signs:

  1. Parkinsonism
  2. Visual Hallucinations
  3. Fluctuating impairment
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14
Q

What is the DOC for Diffuse Lewy Body Dementia?

A

Acetylcholinesterase inhibitors: Rivastigmine or Donepezil

2nd line - Atypical Neuroleptics: Clozapine, Quetiapine, Aripiprazole. (avoid typical like haloperidol due to sensitivity)

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15
Q

Describe Binswanger disease.

A

Subcortical ateriosclerotic encephalopathy. (multiple infarcts in whit matter)

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16
Q

Describe CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)

A

Chromosome 19

Notch 3 gene

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17
Q

Describe frontotemporal dementia

A

Prominent frontal lobe symptoms (less amnestic symptoms)

E.g. - Pick Disease

Behavioral changes initially followed by atrophy of the frontal and anterior lobes.

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18
Q

What is responsible for dementia associated with parkinson disease? Is it idiopathic and coincidental?

A

Lewy body pathology is likely responsible. It is unlikely that it is a coincidence like some suggest.

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19
Q

What are the hallmark signs of parkinson associated dementia?

A

Memory is not as quickly involved. It is more executive dysfunction and visuaospatial impairments, and verbal memory. (FACIAL RECOGNITION)

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20
Q

What test is commonly used to dx PD dementia?

A

MOCA - montreal cognitive assessment for a brief, effective bedside test.

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21
Q

What are some drugs available for the treatment of parkinson related dementia?

A

Rivastigmine (DOC)

Donepezil

Avoid anticholinergic medications.

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22
Q

Describe progressive supranuclear palsy.

A

rare syndrome seen in older folks (45-75y/o)

**Characteristic worried facial expression

Early features: vertical supranuclear gaze palsy with downward gaze abnormalities, and prominent postural instability.

Symmetric onset of bradykinesia and rigidity

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23
Q

Read about dudley moore

A

read now

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24
Q

What is the course of treatment for progressive supranuclear palsy?

A

Treat symptoms due to a definitive treatment being difficult. Most don’t respond to anticholinergic or dopaminergic drugs

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25
Q

List the various forms of reversible dementias?

A

ONLY ABOUT 10% are REVERSIBLE

  1. Normal pressure hydrocephalus
  2. V. B12 deficiency or other deficiency
  3. Hypothyroidism
  4. Syphilis
  5. Meds - may be delirium
  6. Metabolic Disorders
  7. Tumor
  8. Alcohol related
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26
Q

Describe the details of Normal pressure hydrocephalus?

A

Triad of sx: Dementia, Ataxia/Apraxia, Incontinence

“Wet, wacky, wobbly””

No signs of inc. ICP, normal pressure on lumbar puncture.

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27
Q

How is Normal Pressure Hydrocephalus diagnosed?

A

MRI will demonstrate ventriculomegaly.

With NO evidence of CSF flow obstruction

Can be idiopathic or can be caused following subarachnoid hemorrhage or meningitis via imparied CSF absorption or inflammation/fibrosis of the arachnoid granulations

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28
Q

Describe proper treatment of Normal Pressure Hydrocephalus.

A

Shunting

Prognosis can be predicted with lumbar puncture. Outcomes normally better if gait is primarily affected.

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29
Q

Watch all videos in CNS-Dementia Lecture\

Also try to answer questions at end

A

Watch now!

Do questions!

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30
Q

Describe the clinical presentation of Creutzfeldt-Jakob Diesease.

A

Prion caused, rapidly progressing extrapyramidal features, startle induced myoclonus.

CSF 14-3-3 protein will be found.

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31
Q

Describe Chronic Traumatic Encephalopathy.

A

Degenerative brain disease seen with history of concussions.

Triad: Cognitive Impairment, Depression, Irrational and Impulsive Emotional Behavior

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32
Q

What is the pathology/underylying cause of CTE?

A

Abnormal Tau Deposition.

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33
Q

What is sundowning?

A

Increased behavior problems in evening/night

Typically seen in demented, institutionalized patients

Must distinguish from delirium

May need medications or increased lighting in patients environment

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34
Q

Define delirium.

A

Disturbance of consciousness, cognitive change not accounted for by preexisting dementia, develops over short time period, symptoms fluctuate over the day.

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35
Q

Give another definition of delirium?»>«M

A

Acute, transient, potentially reversible confusional state.

Disturbed consciousness and altered cognition.

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36
Q

Which types of procedures see the highest rates of post-op delirium?

A

Cardiac surgery, AAA repair surgery.

Hip Fracture Repair

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37
Q

Describe the “A” Test for inattention.

A

Read a list of letters (up to 60) with the letter A occurring more frequently and in the same tone.

Ask the patient to indicate every time they hear an “A”

Count errors of omission and commission. >2 = abnormal.

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38
Q

Describe treatment for delirium.

A

Environmental modifications
Thiamine
Haloperidol, atypical antipsychotics.

Benzodiazapines - watch out for worsening sx of confusion or sedation.

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39
Q

Describe the symptoms that correlate with certain BAC levels.

A

50-150mg/dl - euphoria, friendliness, impaired concentration/judgement

150-250 - slurred speech, ataxia, anger, diplopia, labile mood, drowsiness

300 - Stupor with combativeness or incoherent speech, vomiting

400 - Coma

500 - Respiratory Paralysis

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40
Q

What is delerium tremens?

A

A syndrome that occurs 48-72 hours after an alcoholic has his last drink.

Causes intense withdrawl symptoms. (tachy, fever, sweating, possibel seizure, possible shock, pneumonia, cirrhosis)

Lasts hours to days

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41
Q

Describe treatment for delerium tremens?

A

Sedation: benzodiazepines, phenobarbital.

Fluids, electrolytes, glucose, nutrition, vitamins, treat underlying condition

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42
Q

Describe wernicke encephalopathy.

A

Acute syndrome****
Alcohol related most often
Thiamine Deficiency (B1)
Neuronal myelin loss, petechial hemorrhages, confusion, impaired memory, inattentiveness, abnormal eye movements, ataxia

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43
Q

What iatrogenic etiology can be seen in wernicke encephalopathy?

A

Giving a thiamine patient IV glucose can precipitate this syndrome

*give alcoholics thiamine IV w/ glucose.

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44
Q

Describe korsakkoff syndrome.

A

CHRONIC CONDITION
Emerges as wernicke encephalopathy clears
Symptoms: retro/antero amnesia, confabulation, impaired insight.

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45
Q

What is the etiology for korsakoff syndrome?

A

lesion in dorsal medial nucleus of thalamus, mamillary bodies, and brianstem.

Usually memory deficits remain even after treatment.

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46
Q

Describe the many alcohol related health complications.

A 
Cerebellar degeneration
Optic Neuropathy 
Peripheral Polyneuropathy 
Myopathy 
Liver Disease
Pellagra
etc>>
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47
Q

Describe hepatic encephalopathy.

A

Altered brain function due to metabolic abnormalities from liver dysfunction.

Symptoms can be reversed after improvement of liver function.

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48
Q

What is the neurotoxin that causes hepatic encephalopathy?

A

Ammonia

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49
Q

What are the symptoms of hepatic encephalopathy?

A

Disturbed sleep, bradykinesia, asterixis, rigidity, hyperactive DTRs

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50
Q

Describe the stages of HE

A

I - euphoria, confusion, sleep disorder

II - Lethargy, confusion, asterixis

III - Marked confusion, slurred speech, sleepy.

IV - Coma

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51
Q

Describe treatment options for Hepatic Encephalopathy.

A

Take care of underlying conditions (GI bleeds, hypovulemia, valproic acid) 70-80 pts. recover after improvements to these.

Reduce serum ammonia - Lactulose, Neomycin

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52
Q

Determine answers to triad questions at end of delirium lecure.

A

DO NOW!

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53
Q

Define sleep

A

physiological state of relative unconsciousness and inaction of the voluntary muscles, the need for which recurs periodically.

Dynamic process.

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54
Q

Describe the 5 stages of sleep.

A 
DEFINED BY EEG (cycles during the night)
I. Light Sleep
II. K-complexes and sleep spindles
III-IV. Slow wave sleep; restorative sleep
REM. Dream Sleep
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55
Q

What serves as the body’s biological clock?

A

suprachiasmatic nucleus

controls cortisol secretion and body temperature

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56
Q

What structures of the brain are important for sleep (other than suprachiasmatic nucleus)?

A

Basal Forebrain
Ant. Hypothalamus
Dorsolateral Medullary Reticular Formation

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57
Q

What are the chemicals important for sleep?

A

Serotonin
Melanocyte stimulating hormone
PGD2
Uridine

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58
Q

What are the leading causes of sleep disorders?

A

Psychiatric disorders (35%)
Insomnia (15%)
Drugs/Alcohol Dependent (12%)
Sleep Apnea (6%)

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59
Q

Describe Transient Insomnia?

A

Several Days Duration
Acute Stress or Environmental Changes
- jet lag, shift work, acute illness, stress, caffeine, alcohol, nicotine

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60
Q

Describe Short-Term Insomnia.

A 
Up to 3 wks Duration
More severe causes than transient. 
- Bereavement
- Emotional Trauma
- Pain
- Marriage
- Divorce
- Moving
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61
Q

Describe Chronic Insomnia.

A

> 3wks. duration
Associated with physical and emotional illness
- Medications, alcohol, illicit drugs.

  • only 10% are substance abusers though
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62
Q

How do you treat insomnia?

A

RESOLVE UNDERLYING PROBLEMS

  • Sleep hygiene
  • Relaxation Training
  • Biofeedback
  • Stimulus control
  • Sleep restriction
  • Cognitive therapy
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63
Q

What are some important considerations prior to Rx of sedating antidepressants for sleep aide.

A

Risk/Benefit analysis
Contraindicated in pt. with BPH or CVD
Use with caution in elderly

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64
Q

What are the common ttreatments for Restless leg syndrome?

A

Anti-Parkinsonian Meds
Benzodiazepine
Opiates
Tricyclic Antidepressants

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65
Q

What is the most common cause of excessive daytime somnolence?

A

Patients are sleepy, have headaches, insomnia, memory troubles, irritability, slow reactions, hypertension, nocturia

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66
Q

What is the chromosome/gene responsible for narcolepsy?

A

Ch. 6 HLA-DR2/DQ1 0602 gene

Deficiency of hypocretin 2 aka orexin B, which is secreted by lateral hypothalamus

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67
Q

Describe sleep walking

A 
aka Somnambulism
Occurs during stage III or IV sleep
Difficult to arouse 
Confusional State 
Susceptible to injury
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68
Q

Describe night terrors

A

aka pavor nocturnus
happens in kids 2 to 12
screaming, crying, intense fear in III/IV sleep
Lasts 3-5 mins

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69
Q

Discuss treatments for pavor nocturnus?

A

Psychotherapy
Guard against injury.
Benzodiazepines

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70
Q

Describe bedwetting

A

aka Nocturnal enuresis
age 4-14 boys>girls
higher incidence if parents are betwetters

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71
Q

What meds can be used for bedwetting?

A

Imipramine for 5mos

DDVAP (desmopressin)

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72
Q

Define coma.

A

Loss of consciousness

Cerebral hemispheres and reticular activating system is needed for consciousness

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73
Q

What does decorticate posturing in a coma represent?

A

thalamus and hemispheres (UPPER) above red nucleus

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74
Q

What does decerebrate posturing in a coma represent?

A

Midbrian lesion

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75
Q

What symptoms will be seen on PE if the causative lesion is in the thalamus or higher?

A

Cheyne-Stokes respiration
Small Reactive Pupils
Decorticate posturing
Brainstem reflexes intact

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76
Q

What symptoms will be seen on PE if the causative lesion is in the midbrain?

A

Central neurogenic hyperventilation
Mid-position fixed pupils
Decerebrate posturing
EOM may be impaired.

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77
Q

What symptoms will be seen on PE if the causative lesion is in the Pons?

A 
Apneustic respiration 
Miotic Pupils (pin point)
Absent EOM
Absent Corneal Reflexes
Flaccidity
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78
Q

What symptoms will be seen on PE if the causative lesion is in the Medulla?

A

Gasping, Apneic resp.
Flaccidity
No Gag
BP/HR irregularities

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79
Q

Define brain death?

A

Absent cerebral and brainstem responses. Apnea, Isoelectric EEG, Absent cerebral blood flow

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80
Q

What are the PEs measured for the Glasgow Coma Scale?

A

Eyes Open

  1. Never
  2. To Pain
  3. Verbal Stimuli
  4. Spontaneously

Verbal responses

  1. None
  2. Incomprensible sounds
  3. Inappropriate words
  4. Disoriented and converses
  5. Oriented

Motor Responses

  1. None
  2. Decerebrate
  3. Decorticate
  4. Flexion withdrawl
  5. Localizes Pain
  6. Obeys
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81
Q

Describe electrolyte imbalances that can cause Neuromuscular weakness.

A

Potassium: 7.0

Calcium 12.0

82
Q

What are the 3 discussed disorders of Neuromuscular Transmission?

A
  1. Myasthenia Gravis
  2. Lambert-Eaton Myasthenic Syndrome
  3. Botulism
83
Q

Describe Myasthenia Gravis?

A

Autoimmune (antibodies directed at Ach receptors)
Associated with thyroid disease, lupus, pernicious anemia, rheumatoid arthritis.
Fluctuating weakness.
Ptosis, diplopia, ocular symptoms, facial, pharyngeal weakness, muscle wasting

84
Q

What is the work-up used in dx of myasthenia gravis?

A

EMG
Tensilon (endrophonium) test
Thorax CT
Ab testing

85
Q

What should be included in a differential of Myasthenia Gravis/

A 
ALS 
Musc. Dystrophy
Lambert-Eaton
Botulism
Organophosphate Poisoning
86
Q

Describe treatment options for Myasthenia Gravis?

A 
Pyridostigmine, neostigmine
Plasmapheresis
IV IgG
Immunosuppressive - steroids, azathioprine, cyclosphamide, cyclosporin
Surgery
87
Q

What is neonatal myasthenia?

A

infants born to myasthenic mothers with weak cry, suck, respiratory insufficiency.

Caused by maternal antibodies

88
Q

Describe Lambert-Eaton Myasthenic Syndrome?

A

Paraneoplastic syndrome
(Small cell lung, breast , lymphoma)
Caused by presynaptic inhibition (voltage-gated Ca2+ channel)

89
Q

What are the symptoms of Lambert-Eaton ?

A

Areflexia, Weakness, Dry Mouth, Metallic Taste, Autonomic Signs.

90
Q

Describe treatment of Lambert-Eaton.

A

IV IgG
Diaminopyridine
Guanidine
Treat Tumor

91
Q

How does botulism cause NMJ symptoms?

A

Presynaptic inhibition of Ach release.

92
Q

What protein is the culprit in Duchenne Muscular Dystrophy?

A

dystrophin

93
Q

Describe duchenne muscular dystrophy.

A

Progressive muscle wasting starting at age 3
Gradual walking difficulty culminating prior to age 11
Toe walking, waddling gait
Growers Sign

94
Q

If a boy can walk reasonably at age 12 what is the likely dx?

A

Becker Muscular dystrophy

95
Q

Describe Becker Muscular Dystrophy.

A

Very similar to duchenne but slower progression.

Wheelchair by 30, die by 50

also x-recessive gene

96
Q

Pt has foot drop, facial/shoulder weakness that appeared in adolescence, Beevor sign, Winging scapula. Dx?

A

Facioscapulohumeral Muscular Dystrophy

97
Q

Describe myotonic dystrophy?

A

aka steinert disease
Chromosome 19
Defect in muscle membrane function

98
Q

What is a syndrome of generalized myotonia which is more severe than myotonic dystrophy?

A

Myotonia Congenita

99
Q

Describe the class of mitochondrial cytopathies.

A

Caused by dysfunction of mitochondria, inherited through mother.

Lactic acidosis, ragged red fibers, lipid droplets

Kearns-Sayre Syndrome, MELAS, MERFF

100
Q

Describe dermatomyositis.

A

Involves skin and muscle
Usually begins with rash and muscle weakness
Muscle aches and proximal weakness.

Sometimes associated with lung, breast, and GI cancers in pt. >40yo

101
Q

Describe polymyositis. How is it differentiated from others?

A

Occurs after 35
No fam history of inherited disorders
**Doesn’t involve extraocular muscles.

102
Q

What are the major glycogen storage diseases?

A

Type II - Pompe - acid maltase deficiency, cardiomyopathy, myopathy, infancy

Type V- McArdles - myophosphorylase deficiency, cramps, intolerance to intense exercise, myoglobinuria

103
Q

Describe the intrinsic mechanism of Parkinson?

A

Dopamine –> Free Radicals –> Lipid Peroxides—-> Membrane dysfunction —> Nigral Damage

104
Q

Describe the extrinsic mechanism of Parkinson?

A

Protoxin (eg. MPTP) —-> Toxin —> Mitochondrial Dysfunction —> Nigral Damage

105
Q

What is the direct cause of intrinsic parkinson?

A

Lipid peroxide damage to nigra via free radicals

106
Q

What is the direct cause of extrinsic parkinson?

A

Protoxins being metabolized to toxin causing mitochondrial dysfunction

107
Q

Describe the patholocical features of Parkinson?

A

Lewy Bodies
Neuronal Loss
Depigmentation of nigra, locus ceruleus, and dorsal vagal nucleus

108
Q

What neuroprotective drug can be used to treat Parkinson?

A

Selegiline - MAOI inhibitor

Avoid use with meperidine, antidepressants, and SSRIs

109
Q

What anticholinergic meds can be used in Parkinson?

A

benztropine, biperiden

help tremor and rigidity

careful in elderly beause of anticholinergic side effects

110
Q

What is a good drug to help tremors in elderly that doesnt possess the side effects of anticholinergics?

A

Amantadine (dopaminergic effect)

111
Q

What dopamine agonists can be used for parkinson?

A

Bromocriptine, pergolide, ropinirole, pramipexole

Can be used instead of or in conjunction with levodopa

112
Q

Describe COMT inhibitors in the treatment of Parkinson?

A

Tolcapone, Entacapone

Enhances levodopa

Watch for liver toxicity**

113
Q

Why is levodopa a good therapy for parkinson?

A

Crosses BBB, converted in brian to dopamine.

114
Q

Why is carbidopa given with levidopa?

A

Inhibits peripheral levodopa metabolism for brain selectivity.

115
Q

Describe dystonia?

A

Sustained contractions that may be rapid and repetitive, focal or generalized, idiopathic or symptomatic

116
Q

What are some treatment options for dystonia?

A

Levodopa, Haloperidol, Phenothiazines

117
Q

Describe Idiopathic Torsion Dystonia.

A 
Age 5-15 
Begins focally (foot inversion)

Spasms distort body
Mentally normal
Disappears with sleep

118
Q

Describe proper treatment for Idiopathic Torsion Dystonia.

A

Diazepam, Anticholinergics, Baclofen, Carbamazepine.

Biofeedback
Surgery (Thalamotomy)

119
Q

What is the most common treatment of the various focal dystonias?

A

Botox or surgery

120
Q

Describe Essential Tremors.

A

Most Common Movement Disorder
Most apparent with stress and outstretched arms.
May involve head and voice

121
Q

Treatments for essential tremors?

A

Alcohol, B-Blocker, Primidone, Pams (lorazapam, diazapam), Pacemakers

122
Q

Describe Tardive dyskinesia?

A

Commonly drug induced
Persistent, often permanent, repetitive, involuntary movements

Mostly lower face and buccal muscles

Chewing, tongue darting, piano playing fingers, marching in place.

123
Q

What drug may be helpful in treatment of Tardive dyskinesia?

A

Reserpine

124
Q

What drugs are behind drug induced parkinsonism?

A

antipsychotics, methyl dopa, metoclopramide

125
Q

What is acute akathisia?

A

Inner feeling of restlessness
Unable to sit still
More often in women

126
Q

What is acute dystonic reaciton?

A

Common in young patients

Responds well to diphendydramine, benztropine, diazepam injection

127
Q

Describe Neuroleptic Malignant syndrome.

A

common in young adults

occurs with antipsychotic treatment.

128
Q

Symptoms of neuroleptic malignant syndrome?

A

autonomic dysfunction, fever, rigidity, akinesia, altered mental status, acidosis, myoglobinuria

129
Q

Describe treatment for Neuroleptic Malignant syndrome?

A

Supportive: drug withdrawl immediately, bromocriptine, dantrolene

130
Q

Describe Sydenham Chorea.

A

aka St. Vitus Dance
self limiting disease of children 5-15
manifestation of rheumatic fever.

131
Q

What is the etiology of Sydenham Chorea?

A

Rheumatic fever resulting in Abs to subthalamic and caudate basal nuclei.

132
Q

What is the treatment for Sydenham Chorea?

A

Sedatives, Phenothaizines, Haloperidol, Valproic Acid.

133
Q

Describe Huntington Chorea?

A

Inherited - chromosome 4p, CAG trinucleotide repeat. coding for huntingtin protein cuasing gain-function mutation.

Loss of GABA and Cholinergic neruons, atrophy of caudate nucleus.

134
Q

Describe treatment for Huntington Chorea

A

Symptomatic

Haloperidol, Phenothiazine, Reserpine, Genetic counseling.

135
Q

Describe hemiballisms.

A

Violent chorea movements caused by a lesion to CL subthalamic nucleus

136
Q

How to treat hemiballisms?

A

same as chorea: Haloperidol, Phenothiazine, Reserpine.

137
Q

What genetic risk factors are specific to likelihood of stroke?

A

Apop E4
Inc. Homocysteine Levels
Factor V mutation

138
Q

What are the most damaging/long lasting cardiogenic emboli?

A

A-Fib derived - larger, longer lasting, more damaging

139
Q

Differentiate between carotid distribution and vertebrobasilar distribution TIAs

A

Carotid: Unilateral***, weak, numb, aphasia, monocular vision loss.

Vertebrobasilar: Bilateral***, weak, numb, visual loss, diplopia, vertigo, ataxia, dysphagia

140
Q

Define Amaurosis Fugax.

A

Partial or complete loss of vision in one eye (like a shade covered the eye).

Seen in TIAs of carotid origin, can be thrombotic or embolic.

141
Q

How do you differentiate TIAs etiology?

A

Single event: could be thromb or embolic

Multiple SImilar EVents: Thrombus

Multiple dissimilar events: Embolic

142
Q

Embolic vs Thrombotic symptoms?

A

Embolic: seizure at onset, focal defect, sudden onset, hemorrhagic transformation

Thrombotic: slow progression, preceded by TIA

143
Q

Describe the symptoms of an ACA occlusion.

A

Hemiplegia and Hemianesthesia mostly in leg, Urinary symptoms, apathy

144
Q

Describe the symptoms of a MCA occlusion.

A

Hemiplegia and Hemianesthesia in face and arm mostly, Homonomous hemianopia, aphasia of dominant hemisphere if affected.

145
Q

Describe Brocas aphasia.

A

Nonfluent, expressive or anterior aphasia.

Difficulty producing speech but understanding is intact.

146
Q

Describe Wernicke Aphasia.

A

Fluent, receptive, posterior aphasia

Impaired comprehension, paraphasia, neoglisms, gibberish.

147
Q

Describe conduction aphasia.

A

Lesion in the arcuate fasciculus. Difficulty with repetition.

148
Q

Describe Global Aphasia.

A

MCA infarct

All aspects affected@!

149
Q

What are the symptoms of PCA occlusion?

A

Homonomous hemianopia

Hemiplegia or hemiparesis

150
Q

What is small vessel disease?

A 
aka lacunar infarcts
Pure motor or pure sensory 
pseudobulbar palsy
dysarthria
hemiataxic, hemiplegic
151
Q

What are biggest risk factors for small vessel diseaes?

A

HTN , Diabetes

MRI preferred for dx

152
Q

Describe treatment for Small Vessel Disease.

A

Control BP
Antiplatelet agents
Carotid Endarterectomy

153
Q

Describe Weber syndrome.

A

CNIII palsy with hemiplegia due to a midbrain stroke.

154
Q

Describe Wallenberg syndrome.

A

Occlusion of vertebral or PICA artery resulting in IL facial numbness, ataxia, Horner’s, Dysphagia, Hoarsness, Loss of taste, Arm/Leg numbness. CL pain/temp loss.

155
Q

What is an ischemic penumbra?

A

Neurons that were damaged/affected by an infarct, but are still viable for rehabilitation.

156
Q

What is the best antiplatelet therapy based on event reduction percentages?

A

Dipyridamole + Aspirin (50mg) = 24%

Aspirin <325mg = 25% reduction

157
Q

Which antiplatelet therapy is recommended if TIA occurs during Aspirin therapy?

A

Clopidogrel

158
Q

What is the best drug for reduction of cardioembolic TIAs?

A

Warfarin

159
Q

What is the DOC for patients with atherothrombotic TIAs?

A

ASA

Dipyridamole+ASA in aspirin intolerant.

160
Q

What should be done is a carotid bruit is found in a patient with no symptoms?

A

Be sure that management is a goal.

Educate patient
Cardiac workup to be safe
Surgery if indicated

161
Q

What drug is used in the 1st 3 hours of an ischemic stroke? Describe it?

A

TPA- Tissue Plasminogen Activator

MAKE SURE THERE ARE NO PRESENT BLEEDS

Converts plasminogen to plasmin resulting in clot busting activity.

If BP >185/110 use BP agent first (labetalol)

162
Q

Describe eclampsia

A

Also known as hypertensive encephalopathy with high BP that can cause headache, confusion, seizures, focal deficits.

Treat with BP agents.

163
Q

Describe transient global amnesia.

A

Sudden loss of memory

Cause is most likely vascular

164
Q

Describe Temporal Arteritis.

A

Seen in 60-80yos

Headache, fever, anorexia, weight loss, blindness. Tender artery

165
Q

What is temporal arterits associated with?

A

polymyalgia rheumatica, stiff aching muscles

Sed rate increased

Treat with steroids

166
Q

Describe vasogenic cerebral edema?

A

Increased capillary perm. results in increased Extracellular Fluid. Associated with tumor or hematoma

167
Q

Describe cytotoxic edema

A

Cellular swelling involving gray and white matter, associated with hypoxia and infarcts

168
Q

Describe Interstitial Edema

A

CSF OBSTRUCTION
Increased periventricular fluid
Seen with hydrocephalus

169
Q

What is cushing’s effect?

A

Increased systolic BP
Decreased HR <60bmp
Altered respiration

170
Q

Describe treatment options for cerebral edema?

A

Hyperventilation
Osmotherapy (mannitol/glycerol)
Steroids
Diuretics

171
Q

What is the most common cause of intraparenchymal hemorrhage?

A

HTN
Rupture of small penetrating arteries
Putamen/Thalamus/ Pons can be affected
Treatment depends on location

172
Q

Most common cause of subarachnoid hemorrhage?

A

Aneurysm or Trauma

Worst headache of life, nuchal rigidity, alert to coma quickly, focal deficits

173
Q

Describe the Hess and Hunt Grading scale for hemorrhages.

A 
I Asymptomatic/Headaches
II. Moderate headache, nuchal rigidity 
III. Drowsy, mild focal deficits
IV. Semicomatose, posturing
V. Deep coma; decerebrate posture
174
Q

What type of aneurysms can be seen in patients with bacterial endocarditis?

A

Mycotic Aneurysm

Septic embolus lodging in vessel wall and can rupture (80% fatal)

175
Q

Most common cause of Epidural Hematoma?

A

Trauma - parietal or temporal fracture
Laceration of MMA

Surgical emergency

176
Q

Describe acute subdural hematoma

A

Comatose from start

tearing of bridging veins due to trauma

177
Q

What are the signs of acute subdural hematoma?

A

Blown pupils, hemiplegia, cushings reflex, altered respirations.

178
Q

Describe chronic subdural hematoma?

A

traumatic even is less evident

mild focal deficits, confusion, headache

179
Q

Describe the difference between a CVA and a TIA.

A

CVA- rapid onset of focal or global symptoms lasting >24 hrs, no apparent cause other than vascular origin. “brain attack”

TIA: same thing

180
Q

What is the ultimate goal of stroke rehabilitation?

A

Return to maximum recovery of physical, cognitive, and psychological function, thereby, optimizing independence, QOL, and dignity.

181
Q

Describe the Twitchell predictions for natural recovery from stroke derived impairments.

A

Immediate: Decreased voluntary movements/MSRs

48hr: Increased MSRs

1-38d: Spacticity/Clonus

6-33d: Increased voluntary movement/ decreased spaciticity

182
Q

Describe the general patterns seen in stroke patients. With regard to motor recovery.

A

Generally regained proximal to distal, and LE recovers faster than UE

Complete paralysis of arm at onset correlates with poor recovery of full hand ROM.

Some movement in hand by 4weeks correlates well with full recovery (70%)

183
Q

Describe what is meant by spasticity?

A

Abnormal velocity-dependent resistance to stretch.

Usually follows classic UE flexor, and LE extensor pattern.

184
Q

Location of lesion for Broca aphasia?

A

L posteroinferior frontal cortex

Non-fluent, comprehensive, non-repetitive.

(Speech generation is the problem)

185
Q

Location of Transcortical Motor aphasia lesion?

A

superior and anterior to broca.

Non-fluent, Comprehensive, Repetitive
PURE MOTOR PROBLEM W/ FLUENCY ISSUES

186
Q

Location of Wernicke aphasia lesion?

A

Left superior temporal, or inferior parietal cortex.

Fluent, non-comprehensive, non-repetitive.

(Can generate speech, but nothing gets processed when it goes in)

187
Q

Location of transcortical sensory aphasia lesion?

A

Posterior inferior to wernicke.

Fluent, non-comprehensive, repetitive

(Language processing only, can repeat, and generate language, but can’t make sense of what they are repeating.)

188
Q

Location of conduction aphasia lesion?

A

left superior temporal or supramarginal gyrus of parietal.

Fluent, comprehensive, non-repetitive.

189
Q

Location of global aphasia lesion?

A

Frontal temporal parietal lobes. Usually complete MCA CVA.

Non-everything

190
Q

Location of anomic aphasia lesion?

A

Left temporal + Parietal areas. Often a result of recovery from another type of aphasia.

Can do everything, just have pauses and circumloculations (the use of many words where fewer would do, especially in a deliberate attempt to be vague or evasive)

191
Q

What are the stroke complications that can present as an aphasia but may be a different deficit?

A

Dysarthria: weakness, paralysis, or a lack of cooridination of the motor-speech system.

Abulia: lack of will or initiative

Apraxia: Deficit in motor planning, not language productio. Lesion located in left anterior corpus callosum.

192
Q

Describe a craniotomy.

A

Skin flap made to expose skull, which is removed to access relevant anatomy. Surgical removal of hematoma, or lesion.

193
Q

What is stereotactic radiosurgery?

A

single, high-dose irradiation to small, critically located intracranial volume through intact skull.

194
Q

What is radiosurgery (gamma knife) used for?

A 
Small lesions (<3cm)
Most commonly used for:

Tumors: Metastasis, meningiomas, acoustic neuromas, pituitary tumors, gliomas.

Vascular: Arteriovenous malformations, dural AV fistulas, Cavernomas

Disorders: Trigeminal Neuralgia, Movement Disorders

195
Q

At what level on the Glasgow scale should a concussion patient be admitted to the hospital?

A

anything less than 15

=15 then monitor through outpatient setting and watch for regression.

196
Q

Describe second impact syndrome.

A

Diffuse cerebral swelling after a second concussion while still symptomatic from first.

Recommended that pt. with concussion lasting more than 15 mins. NOT return to play until asymptomatic for at least 1 week.

Pt. with repeated concussion associated with loss of consciousness or symptoms for 15 mins NOT return to play for the rest of the season.

197
Q

Following a traumatic brain injury. When is it necessary to intubate a patient?

A

GCS <8

198
Q

What needs to be done to treat hypotension associated with a traumatic brain injury?

A

adequate fluid resuscitation w/ isotonic crystalloids.

199
Q

Summarize the intracranial pressure recommendations in severe head injury.

A

Increased ICP associated with increased mortality and worsened outocom.

ICP monitoring indication: GCS <=8; abnormal CT showing evidence of mass effect (hematoma, contusion, swelling)

Ventricular catheter connected to strain gauge transducer.

200
Q

What is an intraventricular cathether?

A

A drainage tube that is inserted into the head trauma pts. right lateral ventricle to monitor ICP during mgmt. of situation.

201
Q

Describe the treatment of elevated ICP in traumatic head injury patients.

A

Osmotic therapy: Mannitol, Hypertonic Saline.

Hyperventilation

Sedation: Propofol, Pentobarbital, thiopental

Neurological System (10 decks)

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