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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
List the various forms of reversible dementias?
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
26
Describe the details of Normal pressure hydrocephalus?
Triad of sx: Dementia, Ataxia/Apraxia, Incontinence "Wet, wacky, wobbly"" No signs of inc. ICP, normal pressure on lumbar puncture.
27
How is Normal Pressure Hydrocephalus diagnosed?
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
28
Describe proper treatment of Normal Pressure Hydrocephalus.
Shunting Prognosis can be predicted with lumbar puncture. Outcomes normally better if gait is primarily affected.
29
Watch all videos in CNS-Dementia Lecture\ Also try to answer questions at end
Watch now! | Do questions!
30
Describe the clinical presentation of Creutzfeldt-Jakob Diesease.
Prion caused, rapidly progressing extrapyramidal features, startle induced myoclonus. CSF 14-3-3 protein will be found.
31
Describe Chronic Traumatic Encephalopathy.
Degenerative brain disease seen with history of concussions. Triad: Cognitive Impairment, Depression, Irrational and Impulsive Emotional Behavior
32
What is the pathology/underylying cause of CTE?
Abnormal Tau Deposition.
33
What is sundowning?
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
34
Define delirium.
Disturbance of consciousness, cognitive change not accounted for by preexisting dementia, develops over short time period, symptoms fluctuate over the day.
35
Give another definition of delirium?>>><
Acute, transient, potentially reversible confusional state. Disturbed consciousness and altered cognition.
36
Which types of procedures see the highest rates of post-op delirium?
Cardiac surgery, AAA repair surgery. Hip Fracture Repair
37
Describe the "A" Test for inattention.
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.
38
Describe treatment for delirium.
Environmental modifications Thiamine Haloperidol, atypical antipsychotics. Benzodiazapines - watch out for worsening sx of confusion or sedation.
39
Describe the symptoms that correlate with certain BAC levels.
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
40
What is delerium tremens?
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
41
Describe treatment for delerium tremens?
Sedation: benzodiazepines, phenobarbital. Fluids, electrolytes, glucose, nutrition, vitamins, treat underlying condition
42
Describe wernicke encephalopathy.
Acute syndrome****** Alcohol related most often Thiamine Deficiency (B1) Neuronal myelin loss, petechial hemorrhages, confusion, impaired memory, inattentiveness, abnormal eye movements, ataxia
43
What iatrogenic etiology can be seen in wernicke encephalopathy?
Giving a thiamine patient IV glucose can precipitate this syndrome *give alcoholics thiamine IV w/ glucose.
44
Describe korsakkoff syndrome.
CHRONIC CONDITION Emerges as wernicke encephalopathy clears Symptoms: retro/antero amnesia, confabulation, impaired insight.
45
What is the etiology for korsakoff syndrome?
lesion in dorsal medial nucleus of thalamus, mamillary bodies, and brianstem. Usually memory deficits remain even after treatment.
46
Describe the many alcohol related health complications.
``` Cerebellar degeneration Optic Neuropathy Peripheral Polyneuropathy Myopathy Liver Disease Pellagra etc>> ```
47
Describe hepatic encephalopathy.
Altered brain function due to metabolic abnormalities from liver dysfunction. Symptoms can be reversed after improvement of liver function.
48
What is the neurotoxin that causes hepatic encephalopathy?
Ammonia
49
What are the symptoms of hepatic encephalopathy?
Disturbed sleep, bradykinesia, asterixis, rigidity, hyperactive DTRs
50
Describe the stages of HE
I - euphoria, confusion, sleep disorder II - Lethargy, confusion, asterixis III - Marked confusion, slurred speech, sleepy. IV - Coma
51
Describe treatment options for Hepatic Encephalopathy.
Take care of underlying conditions (GI bleeds, hypovulemia, valproic acid) 70-80 pts. recover after improvements to these. Reduce serum ammonia - Lactulose, Neomycin
52
Determine answers to triad questions at end of delirium lecure.
DO NOW!
53
Define sleep
physiological state of relative unconsciousness and inaction of the voluntary muscles, the need for which recurs periodically. Dynamic process.
54
Describe the 5 stages of sleep.
``` 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 ```
55
What serves as the body's biological clock?
suprachiasmatic nucleus controls cortisol secretion and body temperature
56
What structures of the brain are important for sleep (other than suprachiasmatic nucleus)?
Basal Forebrain Ant. Hypothalamus Dorsolateral Medullary Reticular Formation
57
What are the chemicals important for sleep?
Serotonin Melanocyte stimulating hormone PGD2 Uridine
58
What are the leading causes of sleep disorders?
Psychiatric disorders (35%) Insomnia (15%) Drugs/Alcohol Dependent (12%) Sleep Apnea (6%)
59
Describe Transient Insomnia?
Several Days Duration Acute Stress or Environmental Changes - jet lag, shift work, acute illness, stress, caffeine, alcohol, nicotine
60
Describe Short-Term Insomnia.
``` Up to 3 wks Duration More severe causes than transient. - Bereavement - Emotional Trauma - Pain - Marriage - Divorce - Moving ```
61
Describe Chronic Insomnia.
>3wks. duration Associated with physical and emotional illness - Medications, alcohol, illicit drugs. - only 10% are substance abusers though
62
How do you treat insomnia?
RESOLVE UNDERLYING PROBLEMS - Sleep hygiene - Relaxation Training - Biofeedback - Stimulus control - Sleep restriction - Cognitive therapy
63
What are some important considerations prior to Rx of sedating antidepressants for sleep aide.
Risk/Benefit analysis Contraindicated in pt. with BPH or CVD Use with caution in elderly
64
What are the common ttreatments for Restless leg syndrome?
Anti-Parkinsonian Meds Benzodiazepine Opiates Tricyclic Antidepressants
65
What is the most common cause of excessive daytime somnolence?
Patients are sleepy, have headaches, insomnia, memory troubles, irritability, slow reactions, hypertension, nocturia
66
What is the chromosome/gene responsible for narcolepsy?
Ch. 6 HLA-DR2/DQ1 0602 gene Deficiency of hypocretin 2 aka orexin B, which is secreted by lateral hypothalamus
67
Describe sleep walking
``` aka Somnambulism Occurs during stage III or IV sleep Difficult to arouse Confusional State Susceptible to injury ```
68
Describe night terrors
aka pavor nocturnus happens in kids 2 to 12 screaming, crying, intense fear in III/IV sleep Lasts 3-5 mins
69
Discuss treatments for pavor nocturnus?
Psychotherapy Guard against injury. Benzodiazepines
70
Describe bedwetting
aka Nocturnal enuresis age 4-14 boys>girls higher incidence if parents are betwetters
71
What meds can be used for bedwetting?
Imipramine for 5mos | DDVAP (desmopressin)
72
Define coma.
Loss of consciousness | Cerebral hemispheres and reticular activating system is needed for consciousness
73
What does decorticate posturing in a coma represent?
thalamus and hemispheres (UPPER) above red nucleus
74
What does decerebrate posturing in a coma represent?
Midbrian lesion
75
What symptoms will be seen on PE if the causative lesion is in the thalamus or higher?
Cheyne-Stokes respiration Small Reactive Pupils Decorticate posturing Brainstem reflexes intact
76
What symptoms will be seen on PE if the causative lesion is in the midbrain?
Central neurogenic hyperventilation Mid-position fixed pupils Decerebrate posturing EOM may be impaired.
77
What symptoms will be seen on PE if the causative lesion is in the Pons?
``` Apneustic respiration Miotic Pupils (pin point) Absent EOM Absent Corneal Reflexes Flaccidity ```
78
What symptoms will be seen on PE if the causative lesion is in the Medulla?
Gasping, Apneic resp. Flaccidity No Gag BP/HR irregularities
79
Define brain death?
Absent cerebral and brainstem responses. Apnea, Isoelectric EEG, Absent cerebral blood flow
80
What are the PEs measured for the Glasgow Coma Scale?
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
81
Describe electrolyte imbalances that can cause Neuromuscular weakness.
Potassium: 7.0 | Calcium 12.0
82
What are the 3 discussed disorders of Neuromuscular Transmission?
1. Myasthenia Gravis 2. Lambert-Eaton Myasthenic Syndrome 3. Botulism
83
Describe Myasthenia Gravis?
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
What is the work-up used in dx of myasthenia gravis?
EMG Tensilon (endrophonium) test Thorax CT Ab testing
85
What should be included in a differential of Myasthenia Gravis/
``` ALS Musc. Dystrophy Lambert-Eaton Botulism Organophosphate Poisoning ```
86
Describe treatment options for Myasthenia Gravis?
``` Pyridostigmine, neostigmine Plasmapheresis IV IgG Immunosuppressive - steroids, azathioprine, cyclosphamide, cyclosporin Surgery ```
87
What is neonatal myasthenia?
infants born to myasthenic mothers with weak cry, suck, respiratory insufficiency. Caused by maternal antibodies
88
Describe Lambert-Eaton Myasthenic Syndrome?
Paraneoplastic syndrome (Small cell lung, breast , lymphoma) Caused by presynaptic inhibition (voltage-gated Ca2+ channel)
89
What are the symptoms of Lambert-Eaton ?
Areflexia, Weakness, Dry Mouth, Metallic Taste, Autonomic Signs.
90
Describe treatment of Lambert-Eaton.
IV IgG Diaminopyridine Guanidine Treat Tumor
91
How does botulism cause NMJ symptoms?
Presynaptic inhibition of Ach release.
92
What protein is the culprit in Duchenne Muscular Dystrophy?
dystrophin
93
Describe duchenne muscular dystrophy.
Progressive muscle wasting starting at age 3 Gradual walking difficulty culminating prior to age 11 Toe walking, waddling gait Growers Sign
94
If a boy can walk reasonably at age 12 what is the likely dx?
Becker Muscular dystrophy
95
Describe Becker Muscular Dystrophy.
Very similar to duchenne but slower progression. Wheelchair by 30, die by 50 also x-recessive gene
96
Pt has foot drop, facial/shoulder weakness that appeared in adolescence, Beevor sign, Winging scapula. Dx?
Facioscapulohumeral Muscular Dystrophy
97
Describe myotonic dystrophy?
aka steinert disease Chromosome 19 Defect in muscle membrane function
98
What is a syndrome of generalized myotonia which is more severe than myotonic dystrophy?
Myotonia Congenita
99
Describe the class of mitochondrial cytopathies.
Caused by dysfunction of mitochondria, inherited through mother. Lactic acidosis, ragged red fibers, lipid droplets Kearns-Sayre Syndrome, MELAS, MERFF
100
Describe dermatomyositis.
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
Describe polymyositis. How is it differentiated from others?
Occurs after 35 No fam history of inherited disorders **Doesn't involve extraocular muscles.
102
What are the major glycogen storage diseases?
Type II - Pompe - acid maltase deficiency, cardiomyopathy, myopathy, infancy Type V- McArdles - myophosphorylase deficiency, cramps, intolerance to intense exercise, myoglobinuria
103
Describe the intrinsic mechanism of Parkinson?
Dopamine --> Free Radicals --> Lipid Peroxides----> Membrane dysfunction ---> Nigral Damage
104
Describe the extrinsic mechanism of Parkinson?
Protoxin (eg. MPTP) ----> Toxin ---> Mitochondrial Dysfunction ---> Nigral Damage
105
What is the direct cause of intrinsic parkinson?
Lipid peroxide damage to nigra via free radicals
106
What is the direct cause of extrinsic parkinson?
Protoxins being metabolized to toxin causing mitochondrial dysfunction
107
Describe the patholocical features of Parkinson?
Lewy Bodies Neuronal Loss Depigmentation of nigra, locus ceruleus, and dorsal vagal nucleus
108
What neuroprotective drug can be used to treat Parkinson?
Selegiline - MAOI inhibitor Avoid use with meperidine, antidepressants, and SSRIs
109
What anticholinergic meds can be used in Parkinson?
benztropine, biperiden help tremor and rigidity careful in elderly beause of anticholinergic side effects
110
What is a good drug to help tremors in elderly that doesnt possess the side effects of anticholinergics?
Amantadine (dopaminergic effect)
111
What dopamine agonists can be used for parkinson?
Bromocriptine, pergolide, ropinirole, pramipexole Can be used instead of or in conjunction with levodopa
112
Describe COMT inhibitors in the treatment of Parkinson?
Tolcapone, Entacapone Enhances levodopa *Watch for liver toxicity***
113
Why is levodopa a good therapy for parkinson?
Crosses BBB, converted in brian to dopamine.
114
Why is carbidopa given with levidopa?
Inhibits peripheral levodopa metabolism for brain selectivity.
115
Describe dystonia?
Sustained contractions that may be rapid and repetitive, focal or generalized, idiopathic or symptomatic
116
What are some treatment options for dystonia?
Levodopa, Haloperidol, Phenothiazines
117
Describe Idiopathic Torsion Dystonia.
``` Age 5-15 Begins focally (foot inversion) ``` Spasms distort body Mentally normal Disappears with sleep
118
Describe proper treatment for Idiopathic Torsion Dystonia.
Diazepam, Anticholinergics, Baclofen, Carbamazepine. Biofeedback Surgery (Thalamotomy)
119
What is the most common treatment of the various focal dystonias?
Botox or surgery
120
Describe Essential Tremors.
Most Common Movement Disorder Most apparent with stress and outstretched arms. May involve head and voice
121
Treatments for essential tremors?
Alcohol, B-Blocker, Primidone, Pams (lorazapam, diazapam), Pacemakers
122
Describe Tardive dyskinesia?
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
What drug may be helpful in treatment of Tardive dyskinesia?
Reserpine
124
What drugs are behind drug induced parkinsonism?
antipsychotics, methyl dopa, metoclopramide
125
What is acute akathisia?
Inner feeling of restlessness Unable to sit still More often in women
126
What is acute dystonic reaciton?
Common in young patients | Responds well to diphendydramine, benztropine, diazepam injection
127
Describe Neuroleptic Malignant syndrome.
common in young adults | occurs with antipsychotic treatment.
128
Symptoms of neuroleptic malignant syndrome?
autonomic dysfunction, fever, rigidity, akinesia, altered mental status, acidosis, myoglobinuria
129
Describe treatment for Neuroleptic Malignant syndrome?
Supportive: drug withdrawl immediately, bromocriptine, dantrolene
130
Describe Sydenham Chorea.
aka St. Vitus Dance self limiting disease of children 5-15 manifestation of rheumatic fever.
131
What is the etiology of Sydenham Chorea?
Rheumatic fever resulting in Abs to subthalamic and caudate basal nuclei.
132
What is the treatment for Sydenham Chorea?
Sedatives, Phenothaizines, Haloperidol, Valproic Acid.
133
Describe Huntington Chorea?
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
Describe treatment for Huntington Chorea
Symptomatic | Haloperidol, Phenothiazine, Reserpine, Genetic counseling.
135
Describe hemiballisms.
Violent chorea movements caused by a lesion to CL subthalamic nucleus
136
How to treat hemiballisms?
same as chorea: Haloperidol, Phenothiazine, Reserpine.
137
What genetic risk factors are specific to likelihood of stroke?
Apop E4 Inc. Homocysteine Levels Factor V mutation
138
What are the most damaging/long lasting cardiogenic emboli?
A-Fib derived - larger, longer lasting, more damaging
139
Differentiate between carotid distribution and vertebrobasilar distribution TIAs
Carotid: Unilateral***, weak, numb, aphasia, monocular vision loss. Vertebrobasilar: Bilateral***, weak, numb, visual loss, diplopia, vertigo, ataxia, dysphagia
140
Define Amaurosis Fugax.
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
How do you differentiate TIAs etiology?
Single event: could be thromb or embolic Multiple SImilar EVents: Thrombus Multiple dissimilar events: Embolic
142
Embolic vs Thrombotic symptoms?
Embolic: seizure at onset, focal defect, sudden onset, hemorrhagic transformation Thrombotic: slow progression, preceded by TIA
143
Describe the symptoms of an ACA occlusion.
Hemiplegia and Hemianesthesia mostly in leg, Urinary symptoms, apathy
144
Describe the symptoms of a MCA occlusion.
Hemiplegia and Hemianesthesia in face and arm mostly, Homonomous hemianopia, aphasia of dominant hemisphere if affected.
145
Describe Brocas aphasia.
Nonfluent, expressive or anterior aphasia. Difficulty producing speech but understanding is intact.
146
Describe Wernicke Aphasia.
Fluent, receptive, posterior aphasia | Impaired comprehension, paraphasia, neoglisms, gibberish.
147
Describe conduction aphasia.
Lesion in the arcuate fasciculus. Difficulty with repetition.
148
Describe Global Aphasia.
MCA infarct | All aspects affected@!
149
What are the symptoms of PCA occlusion?
Homonomous hemianopia | Hemiplegia or hemiparesis
150
What is small vessel disease?
``` aka lacunar infarcts Pure motor or pure sensory pseudobulbar palsy dysarthria hemiataxic, hemiplegic ```
151
What are biggest risk factors for small vessel diseaes?
HTN , Diabetes | MRI preferred for dx
152
Describe treatment for Small Vessel Disease.
Control BP Antiplatelet agents Carotid Endarterectomy
153
Describe Weber syndrome.
CNIII palsy with hemiplegia due to a midbrain stroke.
154
Describe Wallenberg syndrome.
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
What is an ischemic penumbra?
Neurons that were damaged/affected by an infarct, but are still viable for rehabilitation.
156
What is the best antiplatelet therapy based on event reduction percentages?
Dipyridamole + Aspirin (50mg) = 24% Aspirin <325mg = 25% reduction
157
Which antiplatelet therapy is recommended if TIA occurs during Aspirin therapy?
Clopidogrel
158
What is the best drug for reduction of cardioembolic TIAs?
Warfarin
159
What is the DOC for patients with atherothrombotic TIAs?
ASA Dipyridamole+ASA in aspirin intolerant.
160
What should be done is a carotid bruit is found in a patient with no symptoms?
Be sure that management is a goal. Educate patient Cardiac workup to be safe Surgery if indicated
161
What drug is used in the 1st 3 hours of an ischemic stroke? Describe it?
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
Describe eclampsia
Also known as hypertensive encephalopathy with high BP that can cause headache, confusion, seizures, focal deficits. Treat with BP agents.
163
Describe transient global amnesia.
Sudden loss of memory | Cause is most likely vascular
164
Describe Temporal Arteritis.
Seen in 60-80yos | Headache, fever, anorexia, weight loss, blindness. Tender artery
165
What is temporal arterits associated with?
polymyalgia rheumatica, stiff aching muscles Sed rate increased Treat with steroids
166
Describe vasogenic cerebral edema?
Increased capillary perm. results in increased Extracellular Fluid. Associated with tumor or hematoma
167
Describe cytotoxic edema
Cellular swelling involving gray and white matter, associated with hypoxia and infarcts
168
Describe Interstitial Edema
CSF OBSTRUCTION Increased periventricular fluid Seen with hydrocephalus
169
What is cushing's effect?
Increased systolic BP Decreased HR <60bmp Altered respiration
170
Describe treatment options for cerebral edema?
Hyperventilation Osmotherapy (mannitol/glycerol) Steroids Diuretics
171
What is the most common cause of intraparenchymal hemorrhage?
HTN Rupture of small penetrating arteries Putamen/Thalamus/ Pons can be affected Treatment depends on location
172
Most common cause of subarachnoid hemorrhage?
Aneurysm or Trauma | Worst headache of life, nuchal rigidity, alert to coma quickly, focal deficits
173
Describe the Hess and Hunt Grading scale for hemorrhages.
``` I Asymptomatic/Headaches II. Moderate headache, nuchal rigidity III. Drowsy, mild focal deficits IV. Semicomatose, posturing V. Deep coma; decerebrate posture ```
174
What type of aneurysms can be seen in patients with bacterial endocarditis?
Mycotic Aneurysm | Septic embolus lodging in vessel wall and can rupture (80% fatal)
175
Most common cause of Epidural Hematoma?
Trauma - parietal or temporal fracture Laceration of MMA Surgical emergency
176
Describe acute subdural hematoma
Comatose from start | tearing of bridging veins due to trauma
177
What are the signs of acute subdural hematoma?
Blown pupils, hemiplegia, cushings reflex, altered respirations.
178
Describe chronic subdural hematoma?
traumatic even is less evident mild focal deficits, confusion, headache
179
Describe the difference between a CVA and a TIA.
CVA- rapid onset of focal or global symptoms lasting >24 hrs, no apparent cause other than vascular origin. "brain attack" TIA: same thing
180
What is the ultimate goal of stroke rehabilitation?
Return to maximum recovery of physical, cognitive, and psychological function, thereby, optimizing independence, QOL, and dignity.
181
Describe the Twitchell predictions for natural recovery from stroke derived impairments.
Immediate: Decreased voluntary movements/MSRs 48hr: Increased MSRs 1-38d: Spacticity/Clonus 6-33d: Increased voluntary movement/ decreased spaciticity
182
Describe the general patterns seen in stroke patients. With regard to motor recovery.
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
Describe what is meant by spasticity?
Abnormal velocity-dependent resistance to stretch. Usually follows classic UE flexor, and LE extensor pattern.
184
Location of lesion for Broca aphasia?
L posteroinferior frontal cortex Non-fluent, comprehensive, non-repetitive. (Speech generation is the problem)
185
Location of Transcortical Motor aphasia lesion?
superior and anterior to broca. | Non-fluent, Comprehensive, Repetitive PURE MOTOR PROBLEM W/ FLUENCY ISSUES
186
Location of Wernicke aphasia lesion?
Left superior temporal, or inferior parietal cortex. Fluent, non-comprehensive, non-repetitive. (Can generate speech, but nothing gets processed when it goes in)
187
Location of transcortical sensory aphasia lesion?
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
Location of conduction aphasia lesion?
left superior temporal or supramarginal gyrus of parietal. Fluent, comprehensive, non-repetitive.
189
Location of global aphasia lesion?
Frontal temporal parietal lobes. Usually complete MCA CVA. Non-everything
190
Location of anomic aphasia lesion?
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
What are the stroke complications that can present as an aphasia but may be a different deficit?
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
Describe a craniotomy.
Skin flap made to expose skull, which is removed to access relevant anatomy. Surgical removal of hematoma, or lesion.
193
What is stereotactic radiosurgery?
single, high-dose irradiation to small, critically located intracranial volume through intact skull.
194
What is radiosurgery (gamma knife) used for?
``` 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
At what level on the Glasgow scale should a concussion patient be admitted to the hospital?
anything less than 15 =15 then monitor through outpatient setting and watch for regression.
196
Describe second impact syndrome.
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
Following a traumatic brain injury. When is it necessary to intubate a patient?
GCS <8
198
What needs to be done to treat hypotension associated with a traumatic brain injury?
adequate fluid resuscitation w/ isotonic crystalloids.
199
Summarize the intracranial pressure recommendations in severe head injury.
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
What is an intraventricular cathether?
A drainage tube that is inserted into the head trauma pts. right lateral ventricle to monitor ICP during mgmt. of situation.
201
Describe the treatment of elevated ICP in traumatic head injury patients.
Osmotic therapy: Mannitol, Hypertonic Saline. Hyperventilation Sedation: Propofol, Pentobarbital, thiopental

Neurological System (10 decks)

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