Exam 4 Flashcards
(415 cards)
1
Q
Vertigo
A
Symptom of illusionary movement
Caused by asymmetry of the vestibular system
2
Q
Most important part of history is someone who is dizzy
A
Timing
Recurrent/monophonic
Length
Triggers
Associated symptoms
3
Q
Central lesions causing vertigo
A
Cerebellum or brainstem
4
Q
Peripheral lesions causing vertigo
A
Labyrinth or vestibular nerve
5
Q
Vertigo examination
A
Eye movements
HINTS
Dix-Hallpike
Vestibular Ocular Reflex
Hearing- Weber and Rivne, CALFRAST
6
Q
HINTS testing
A
Head Inpulse
Nystagmus
Test of Skew
Used to determine if lesion is central or peripheral
7
Q
An abnormal HITS test indicated _ problem
A
Peripheral
8
Q
Nystagmus in a peripheral problem
A
Unidirectional nystagmus
Typically horizontal with torsional component
9
Q
Nystagmus with a central problem
A
Can reverse direction
Can be in any direction (purely vertical/purely horizontal= central sign)
10
Q
Visual fixation with peripheral problem
A
Suppression
11
Q
Visual fixation with central problem
A
Not suppressed
12
Q
Test of Skew
A
Cover uncover test
Look for skew deviation
13
Q
Central vs peripheral vertigo
A
14
Q
Central causes of vertigo
A
Acute stoke
15
Q
First step in management of vertigo
A
If central, MRI to localize and determine next steps
16
Q
Acute central vertigo is _ until proven otherwise
A
stroke
17
Q
Abnormal HINTS exam
A
Brain MRI
18
Q
Acute stroke/TIA management
A
Vascular imaging
Thrombolyic therapy, mechanical thrombectomy, antiplatelet
Manage risk factors
19
Q
Benign Paroxysmal positional vertigo
A
Peripheral cause of vertigo
Recurrent brief episodes of vertigo triggered by head movement
May be associated with nausea/vomiting
Caused by otoliths in semicircular canals causing excessive movement of endolymph
Confirm diagnosis with Dix-Hallpike test
Epley maneuver relieves symptoms
20
Q
Vestibular migraine
A
Another cause of central vertigo
21
Q
Did-Hallpike maneuver
A
Used to detect BPPD
22
Q
Interpretation of Dix Hall Pike test
A
23
Q
Ménière’s disease
A
Peripheral vertigo
Episodic vertigo, tinnitus, and hearing loss
Unilateral sensorineural hearing loss with aural fullness
Commonly idiopathic
24
Q
Vestibular neuritis
A
Peripheral cause of vertigo
Includes vestibular neuronitis and labrynthitis
Sudden onset sever vertigo for 1-2 day follow by gradual resolution
Hearing preserved= vestibular neuronitis
Hearing loss= labrynthitis
25
The NMJ synapse is only
Excitatory
26
Process at NMJ
Ach is released and binds to the receptor on post synaptic membrane causing Na channels to open
Na influx generates AP if threshold is reached
the AP causes the release on Ca ions
Ca binds to tropinin initiating contraction
Ach is degraded by acetylcholinesterase
27
Pre synaptic NMJ disorders
Lambert-Eaton syndrome
Botulism
28
Post synaptic membrane disorders
Myasthenia gravis
29
Presentation of NMJ disorders
Motor complaints
Pure motor
30
Myasthenia gravis is a _ disease
autoimmune
31
Must common antibody in myasthenia gravis
AChR
32
Common presentation myasthenia gravis
Variable weakness and fatiguability of striated voluntary muscle (ptosis gets worse throughout the day)
Ocular with pupil sparing
Bulbar and respiratory dysfunction
Axial and proximal limbs affected more
33
Myasthenia gravis neuro exam
Ocular signs: Ptosis/diploplia with upward gaze, Weakness of eyelid closure
Bulbar signs: jaw weakness, facial diplegia, palatial weakness, tongue weakness
Respiratory signs: respiratory rate, use of accessory muscle, ease of speech and neck strength
Limb strength
Deep tendon reflex
34
Most sensitive test for myasthenia gravis diagnosis
Single fiber EMG
AChR is most specific
35
Myasthenia gravis diagnosis
Ice pack test
ACh receptor antibodies (block active site, damage receptors with help of complement)
MuSK antibodies (IgG4 does not bind complement)
36
End plate potential is generated
At the NMJ after a single nerve action potential (NAP)
37
Muscle action potential is
The propagated potential of a single muscle fiber
38
Compound Muscle Action Potential is
The sum of all the MAPs in a muscle
39
Safety factor
Excess Ach is released beyond what is needed to generate an end plate potential
40
Myasthenia neurophysiology
Some thresholds not met
Slow rate on repetitive nerve stimulation
Jitter and blocking on single fiber EMG
41
Myasthenia treatment
Pyridostimige (inhibits AChE)
Immunosuppressives
Thymectomy
Plasmapheresis
IVIG
42
Myasthenia crisis
Respiratory difficulties
Sever bulbar/respiratory weakness and no cardiac involvement
Treat with IVIG
43
Myasthenia can be related to which cancer?
Thymoma
Need CT/MR chest
Mandatory thymectomy
44
MuSk+ MG
Young females
Sever bulbar, respiratory
Poor response to pyridostigmine
Normal/atrophic thymus
treat with steroids
45
MG in pregnancy
Avoid mycophenolate due to malformation risk
46
Lambert Eaton myasthenic syndrome
Proximal and generalized weakness
Cholinergic dysautonomia
Decreased or absent deep tendon reflexes
50% paraneoplastic
Diagnosis: + P-Q type VGCC and NCS
Treat: 3,4 DAP
47
Botulism
Wound, foot, infantile, inhalational
Degrades proteins necessary for docking/fusion of ACh vesicles preventing release into synaptic cleft
Symptoms: dysphasia, xerostomia, dysarthria, progressive muscle weakness
Tests: look for toxin
EMG/NCS: low compound muscle action potential
Treat: botulism antitoxin, antibiotics
48
Infantile botulism can be caused by
Honey
49
Presynaptic NMJ disorders
Decrement
Facilitation with fast stimulation
50
Myasthenia gravis vs LEMS vs Botulism
51
52
ALS is characterized by the deterioration
of cortical motor neurons, lower brainstem, and the anterior horn cells
53
Death in people with ALS is caused by
Respiratory weakness leading to death
54
ALS risk factors
Family history
Male gender
55
Pathophysiology of ALS
Oxidative stress
Glutamate excitotoxicity
Mitochondrial dysregulation
Prion-like protein dysregulation
56
Pathology of ALS
TDP-42 inclusions cause frontotemporal lobar degeneration
57
ALS symptoms
Focal/regional asymmetric limb onset
Bulbar symptoms
Fasciculations of tongue/limb muscles
Cramps
Spasticity
Weight loss
Muscle loss
Fatigue
SOB/dyspnea/othopnea
Cognitive impairment (frontal temporal dementia)
Parkinsonism
58
This that do not indicate ALS
Pain
Sensory loss
Loss of sphincter tone
59
ALS diagnosis is based on
UMN and LMN involvement
Progressive weakness
Excision of alternate diagnosis
60
Familial ALS
AD inheritance
C9orf72 expansion
SOD mutation
61
ALS management
Riluzole
Sodium phenylbutyrate/taurursodiol
Non-invasive ventilation
Peg-tube
Symptom management
62
ALS prognosis
3-5 years after symptom onset (death from respiratory failure)
63
Primary lateral sclerosis
Affects central motor neurons
No atrophy, fasciculations, or EMG abnormalities
Weakness/spasticity
64
Progressive muscular atrophy
LMN dysfunction
65
Progressive Bulbar palsy
Symptoms in bulbar muscles (innervated by CN IX-XII) due to bilateral LMN impairment
Dysarthria, dysphasia, weight loss
Napkin/handkerchief sign
Progress to involve limbs
66
ALS/parkinsonism-dementia complex
Gait disturbances
Hyperreflexia and limb muscle atrophy
Ridgid-akinetic Parkinsonism and severe dementia
67
Kennedy disease
C-linked trinucleotide CAG repeat (>36) expansion of the androgen receptor gene
Weakness/atrophy affecting facials bulbar, and limb muscles (cramps)
Endocrine disruptions
Female carriers may experience mild symptoms
68
Kennedy disease diagnosis
High HbA1c, CK mildly elevated
genetic confirmation of AR expansion
Supportive treatment
69
Spinal muscular atrophy
Most common fatal genetic disease in infancy
Homozygous deletion or point mutation of SMN1 gene (AR)
Neurodegeneration of anterior horn cell in spinal cord/ brain stem
70
Spinal muscular atrophy manifestations
Tongue atrophy with fasciculations
Hypotonia
Fine tremor
Proximal weakness and atrophy
Waddling gait
Impaired swallowing and ventilatory insufficiency
Kyphoscoliosis
71
Spinal muscular atrophy diagnosis
Genetic confirmation
Supportive care: bipap, tracheostomy
72
West Nile virus
Acute flaccid paralysis
Meningo-encephalitis
73
West Nile virus diagnosis
Regional and asymmetric flaccid paralysis
No pain or sensory deficits
+/- respiratory failure
CSF IgM is diagnostic
EMG: regional/asymmetric MND
74
Acute Flaccid Myelitis
Acute focal onset limb weakness
Caused by coxsackievirus/enterovirus
75
Mixed UMN/LMN is classic for
ALS
76
Chronic focal/regional limb onset
ALS
77
Acute segmental with asymmetry
West Nile virus
Acute flaccid myelitis
78
Chronic symmetric, generalized, proximal>distal
Spinal muscular atrophy
79
Chronic limb and bulbar LMN weakness
Kennedy’s disease
80
Alzheimer’s disease pathology
Brain atrophy (frontal, temporal, parietal)
Narrowing gyri, sulcal widening, atrophic hippocampus, ventricular enlargement
81
Alzheimer’s disease microscopic findings
Plaques (B-amyloid in neutrophils)
Neurofibrillary tangles (tau in neurons
Accumulation due to excessive production/defective removal
82
Familial Alzheimer’s
APP mutation
83
What is the initiating event for the development of Alzheimer’s
B-amyloid accumulation
84
Biomarkers for Alzheimer’s disease
Fluorine 18-amyloid PET scan
p-tau and reduced AB
Blood
85
Alzheimer’s disease treatment
Anti-amyloid antibodies
86
B. Amyloid inclusions
Amyloid plaques
87
Tau inclusions
Neurofibrillary tangles
88
Cerebral amyloid angiopathy
89
Frontotempotal lobar degeneration
Alteration in personality, behavior, language preceding memory loss
Early onset
FTLD-tau, FTLD-TDP
90
FTLD-tau (Pick’s disease)
Only tau
May be caused by mutation in MAPT
91
FTLD-TDP
Frontal and temporal atrophy
Abnormal TDP43 (RNA binding protein)
Mutations in c9orf72 (expansion), TARDBP, GRN
92
ALS
Degeneration of corticospinal tracts
Loss of UMN and LMN
Mutations in C9orf72, SOD 1, TARDBP
93
Parkinson’s disease
Loss of dopamine producing neurons in substantia nigra
Parkinsonism
Lewy bodies (a-synuclein)
SMCA mutation
94
Diffuse Lewy body disease
Dementia associated with PD
Lewy bodies in cortical neurons
95
Myopathy
Muscle weakness
May also have:
Myalgias, cramps, stiffness
Rhabdomyolysis/myoglobinuria
Myotonia
Muscle Atrophy
96
Myopathies can be
Hereditary (muscular dystrophies, congenital myopathies, myotonies, channelopathies, metabolic myopathies, mitochondrial myopathies)
Or
Acquired (inflammatory, endocrine, drug induced/toxic, associated with systemic illness)
97
Labs for myopathy
CK
Aldolase
AST, ALT
Gamma GT
98
Inflammatory myopathies
Dermatomyositis
Inclusion body myositis
Polymyositis
Overlap syndrome
Necrotizing autoimmune myopathy
Infectious
99
Dermatomyositis
100
Inclusion body myositis
101
Muscle weakness pattern in inflammatory myopathies
102
Most common myopathy after 50
Inclusion body myositis
103
Proximal muscle weakness of forearm and thigh atrophy
Inclusion body myositis
104
Polymyositis vs Dermatomyositis vs inclusion body myositis
105
Necrotizing autoimmune myopathy
Subacute severe progressive proximal weakness
Very high CK
Anti-SRP, anti-HMGCoA, connective tissue disease and paraneoplastic
induced by statins
Early aggressive dual immunotherapy improves prognosis
106
Steroid myopathy
Endocrine myopathy
Due to prednisone >30 mg/day
Fluoridated steroids are worse
Proximal muscle weakness
Normal CK, myopathies EMG without active denervation
107
Hyperthyroidism and hypothyroidism can both cause
Endocrine myopathies
108
Hyperthyroidism myopathy
CPK normal
Proximal weakness, periodic paralysis
109
Hypothyroidism
Endocrine myopathy
Proximal weakness, muscle hypertrophy
Ankle jerks=delayed relaxation
Myoedema
110
Vitamin D deficiency may cause
Endocrine myopathy
111
Critical illness myopathy
Associated with sepsis, organ failure, systemic inflammation
Systemic flaccid limb weakness (proximal>distal)
Failure to extubate
112
Muscle dystrophy
Progressive weakness and wasting
Fiber size variation, fibular necrosis and regeneration
Fibrosis and fatty replacement
113
Muscular dystrophies
114
Age of onset muscular dystrophy
115
Largest protein in the human body
Dystrophin
116
Dystrophinopathies
Proximal weakness, neck extensor weakness, calf hypertrophy, lordotic posture, toe walking, waddling gate
117
Duchenne vs Becker
118
Dermatomyositis
119
Dystrophinopathies
120
Steroids are used in which muscular dystrophy?
Duchenne
121
Most common dystrophy in adults
Myotonic dystrophy
-difficulty releasing
122
Myotonic dystrophy: distal pattern with facial weakness
123
Myotonic dystrophy diagnosis
CK normal-mildly elevated
EMG
Muscle biopsy
Genetic testing: >50 CTG repeats C19
124
Myotonic dystrophy treatment
125
Rhabdomyolysis
Acute muscle necrosis and release of intracellular muscle constituents
Triad muscle pain, weakness, dark urine
CK 1500-100,000, myoglobinuria
126
Rhabdomyolysis treatment
Stop offending agent
Hydration, monitor kidney function
127
Recurrent Rhabdomyolysis can be caused bt
CPTII deficiency
128
Metabolic myopathies
Dynamic symptoms: exercise intolerance with muscle pain and cramps
Worsen due to increased physiologic stress
Disorders of glycogen,, lipids, mitochondrial muscle
129
Glycogen vs lipid storage Rhabdomyolysis
130
Mitochondrial myopathy
Hearing loss, short stature, myopathy and peripheral neuropathy
Can be:
Isolated myopathy
Chronic progressive external ophthalmoplegia or Kearns-Sayre syndrome
Encephalopathy of infancy and childhood
Multisystem disease with myopathy (MELAS, MERRF)
131
Acute weakness with CK >5-10K
Rhabdomyolysis
132
Subacute-chronic with rapid progression and high CK
Auto-immune myositis
133
Peripheral nerve disorders affect
Root
Plexus
Nerve
134
Monomelic conditions
Mononeurophathy
Plexopathy
Radiculopathy
135
Polymelic
136
Radiculopathy
Degenerative disease of spine or disc herniation
Pain and mild sensory loss in root distribution
Inflammatory/infectious/neoplastic
Commonly C7, L5
Exam: reflex abnormalities
137
Plexopathy
Single limb with motor, sensory, reflexes impaired
Due to trauma (MVA, penetrating injuries, contact sports, birth trauma), tumor (pancoast), delayed radiation injury, plexitis, Parsonage-Turner syndrome
Can be painful or painless
138
Birth trauma may cause which Plexopathy condition
Erb’s palsy
139
Mononeuropathy
Diabetes, amyloidosis, peripheral neuropathy, hypothyroidism, HNPP
Can cause sensory or motor symptoms
140
Mononeuropathy vs Radiculopathy
141
Most common cause of peripheral neuropathy
Diabetes
142
Approach to polyneuropathy
What: fibers affected/loss of function
When: onset and temporal evolution
Where: length dependent vs non-length dependent
What setting: young- genetic, elderly-idiopathic, middle age-acquired
143
Small fiber vs large fiber neuropathy
144
Painful polyneuropathy with Mee’s lines
Chronic arsenic or thallium poisoning
145
Asymmetric sensory neuropathy with predilection to could skin areas and skin ulceration
Leprous neuropathy
146
Vitamin B12 deficiency and pernicious anemia
147
POEMS
148
Axonal neuropathies
149
Demyelinating neuropathies
150
Polyneuropathy labs
151
Diabetic neuropathy is usually
Distal symmetric large fiber sensorimotor
152
Polyneuropathy treatment
Foot inspections
Medications: Gabapentin, Pregambalin
B12 replacement, diabetes control, alcohol reduction, immunotherapy, infection treatment, cancer or blood dyscrasia treatment
153
Toxic neuropathy
Painful axonal peripheral neuropathy
Timely linked to exposure
154
Most common inherited neuropathies
Charcot-Marie-Tooth type 1a
Distal sensory is predominant phenotype
155
156
157
Polyradiculoneuropathy vs Polyneuropathy
158
Most common cause of acute generalized paralysis
GBS
159
GBS is caused by
Molecular mimicry due to preceding infection
160
GBS presentation
Weakness, Paresthesia, areflexia
Symmetric weakness
161
GBS diagnosis
162
Ganglionopatheis
Asymmetric, non length dependent sensory impairment
Rapid onset, subacute progression
Sensory ataxia
Autoimmune, toxic, infectious, paraneoplastic
163
GBS treatment
Plasma exchange
IVIG
164
Multiple mononeuropathies
Abrupt onset and painful, step-wise subacute progression
Asymmetric
Weakness and sensory loss mapped to multiple nerve territories
Commonly caused by Vasculitis
165
_ is an enduring emotional tone
Mood
166
_ is the physical expression of a person’s immediate felling state, typically focusing on facial expression
Affect
167
Euthymic
Normal mood
168
How thoughts are put together-structure
Thought process
169
Circumstantial thought process
Coherent but over inclusive
170
Tangential structure
Coherent but drifts away from topic
171
Flight of ideas
Rapidly shifting from one idea to another
172
Loose associations
Incoherence
173
Insight
Ability to understand the current situation and implications of various choices
174
Judgement
Decision making
175
Depression diagnosis
depressed mood or anhedonia
plus 4 of the following: SIGECAPS
176
Which health condition can present like major depressive disorder
Hypothyroidism
177
Major depressive disorder diagnosis
At last 1 major depressive episode
No history of mania or hypomania
Use screening tools: PHQ-2,9, Edinburgh depression scale
178
Major depressive disorder specifiers
Psychotic features (in severe depression)
179
Pathophysiology of major depressive disorder
Increased blood flow/decreased volume to prefrontal cortex
Decreased slow wave sleep, decreased REM latency, increased REM sleep
Abnormal variation in cortisol production and non-suppression of cortisol production
Decreased serotonin
180
Natural course of major depressive episode
Resolves in 6 months
50% chance of recurrence
75% risk of recurrence
>95% risk
181
Persistent Depressive Didorder
Depressed mood for majority of 2 years
2 SIGECAPS symptoms
Cannot be symptom free for more than 2 months
Never experiences a manic or hypomanic episode
182
Substance/medication induced depressive disorders
Major depressive episode which starts during or soon after intoxication or withdrawal of a substance
183
Premenstrual Dysphoric Disorder
1 of the following symptoms: lability, anger, depressed mood, anxiety
1 of the following: anhedonia, problems concentrating, low energy, appetite changes, sleep changes, physical symptoms
Most have 5 total symptoms combined
184
Depressive disorder due to another medical condition
Depressed mood/anhedonia
185
Adjustment disorder
Development of emotional/behavior dysfunction in response to a stressor which starts within 3 months of the onset of the stressor
186
Bereavement
Normal low mood in response to an acute loss
187
Treatment of mild depression
Psychotherapy
Exercise
188
Treatment of moderate and serve depression
Medications
Therapy
189
Treatment resistant depression
Electroconvulsive treatment (ECT)
190
SSRI side effects
GI side effects
Bleeding
Hypotnatremia
Sexual side effects
Increased suicide risk
191
SNRIS can also cause
Excessive sweating
Dry mouth
Insomnia
192
NDRI
Can increase anxiety or cause weight loss
193
TCA side effects
Anticholinergic effects
Bleeding risk
QT prolongation and arrhythmias
Sedation
Suicidal thoughts
Lethal in overdone
194
MAOIs
Can cause hypertensive crisis
Must eat low tyramine diet
195
To have a bipolar disorder there must be
A manic or hypomanic episode
196
Major depressive disorder in adolescents
Do not have to be depressed- may be irritable
Do not have to loos/gain weight- consider failure to make expected weight gain
197
Empirical treatments for depression in adolescents
SSRI (fluoxetine-Prozac)
CBT
interpersonal therapy for adolescents
198
Gold standard medication for pediatric population
Fluoxetine (Prozac)
199
Atypical/non-SSRI antidepressant efficacy in adolescents
No better than placebo
200
Optimal treatment for adolescent depression
Combination treatment
201
Mania vs hypomania
Mania- more than 1 week, or any duration if hospitalization is necessary
Hypomania- lasts at least 4 consecutive days
202
Mania criteria
203
Bipolar disorder onset
Most between 15-19 years
Prepubertal onset should be considered unlikely
204
Bipolar disorder treatment
Medications (atypical antipsychotics)
205
Elements of consciousness
Reactivity (arousal) and content (awareness)
206
Disorders of reactivity
Somnolence
Stupor
Coma
207
Disorders of content
Delirium
208
Structural causes of coma
Brainstem or diffuse cortical damage
209
Non-structural causes of coma
Toxic
Metabolic
Electrical
210
Next step for patient in coma
Semiology and imaging (CT)
211
Semiology
212
Oculi-Cephalic reflex
Tests connection between midbrain and pons
213
Bilateral damage between cortex and red nucleus
Decorticate posturing
214
Bilateral damage below the red nucleus
Decerebrate posturing
215
Coma mimics
Locked-in state
fulminant Guillain-Barré syndrome
Akinetic mutism
Catatonia
Psychogenic come
216
Delirium
Deficits in attention
Altered arousal
Symptoms of psychosis
Fluctuate in presence and severity
Medical/surgical triggers
Predisposing factors
217
Brain death
Complete absense of brain function
Irreversible damage of brainstem
Must do imaging to find clear cause (ICH, malignant MCA infarct, DAH, severe TBI, Cardiac arrest)
Absence of confounders
218
Testing for brain death
Apnea test
Nuclear medicine
TCB
EEG vascular studies
219
Aphasia
Impairment of language
220
Dysarthria
Disorder of speech production
221
Leading cause of aphasia
Stroke
222
Dysarthria is common in
Neurologic conditions
223
Developmental langue disorder
Problems in children that impact language production or understanding
224
Speech sound disorder
Speech disorder (ex. Stuttering)
225
Occlusion of a branch of the middle cerebral artery in the inferior lateral frontal lobe
Broca’s area
226
Non fluent aphasia
Broca’s aphasia
227
Wernicke’s aphasia
Fluent aphasia
228
Watershed infarcts
TCM, TCS Aphasia
229
Damage to the accurate fasciculus
Inability to repeat
230
Dorsal streams
Sensorimotor integration
231
Ventral steam
Speech comprehension
232
Global aphasia
Inability to understand and produce words
233
Aprosodias
Right hemisphere, non-verbal aspects of speech and language
234
Alecia without a graphic
Right homonymous hemianopia
235
Dysarthria
Motor speech disorder due to breakdowns in muscle groups used for respiration, phonation, articulation, resonation, or prosody
236
Spastic dysarthria
Strained, strangles, slurred and slow speech, monotone
UMN lesion
237
Flaccid dysarthria
Poor articulation
LMN
238
Ataxic dysarthria
Irregular articulation, variable duration, poor voice and volume control, drunk speech
Dysfunction of cerebellum
239
Hypokinetic dysarthria
Hypophonia, decreased articulation, mono pitch
Basal ganglia dysfunction
240
Aphasia treatment
Speech and language therapy
Compensatory approaches
Early identification and intervention
Lee Silverman voice treatment
241
Dementia
Decline in cognitive abilities leafing to impairment of functional abilities
Chronic
242
Causes of delirium
Metabolic, toxic, sepsis, ICP
243
Dementia types
Alzheimer’s
Vascular
Lewy body
Frontotemporal
244
Dementia staging
245
Amyloid plaques and Neurofibrillary changes
Alzheimer’s
246
Alzheimer’s disease
Gradual onset/progression
No weakness or sensory loss
247
Vascular dementia
Sudden onset, step-wise decline
Focal motor, sensory, reflex changes
Focal cognitive impairment
Vascular disease on brain imaging
Prevention: stroke treatment
248
Vascular dementia subtypes
Small vessel
Large vessel
Mixed
249
Subcortical dementia
Impaired executive cognitive function, visual spatial abilities, memory retrieval
Two core features: extrapyramidal features, fluctuating cognition, visual hallucinations, REM sleep behavior disorder
Faster progression, restless leg syndrome
250
Frontotemporal dementia
Behavioral changes
Diagnosis supported by neuropsychological testing and structural/functional brain imaging
Caused by tau or TDP-43
251
Pick’s disease
252
FTD imaging findings
Atrophy of frontal lobes
Decreased glucose metabolism in frontal lobes
253
Normal pressure hydrocephalus
Gait apraxia
Cognitive impairment
Incontinence
Tap test diagnosis
Treat with VP shunt
Must have evidence of hydrocephalus
254
CJD
Rapidly progressive dementia
Movement disorder
Prion disorder
255
Dementia workup
H&P
Lab tests
Brain imaging
MoCA
256
Lewy bodies
Parkinson’s
Lewy body dementia
257
258
Alzheimer’s biomarkers in CSF
Low amyloid beta
High tau
259
Alzheimer’s risk factors
Age
Genetics- PSEN1/2, APP, APOE4
Lifestyle
260
Cholinesterase inhibitors
Increase Ach by inhibiting acetylcholinesterase
First approved drug for Alzheimer’s
For mild-moderate dementia
Do not prevent progression (moderate improvement)
Side effects: bradycardia, avoid in peptic ulcer disease)
261
Memantine
Moderate-severe AD
NMDA receptor antagonist
Inhibits glutamate
262
Aducanumab
Not very effective
Can cause microhemorrhages, edema
263
Medication approved for Parkinson’s disease dementia
Rivastigmine
264
Mild cognitive impairment medication
SSRI
265
Behavior and psychological symptoms of dementia
Aggression
Agitation
Apathy
Depression
Psychosis
266
The DICE approach
Describe
Investigate
Create
Evaluate
Non-pharmacologic strategies for dementia
267
Antipsychotics are best reserved for
Troubling psychotic symptoms
268
Non-pharmacological strategies for Alzheimer’s
Structure
Children
Pets
Music
Aromatherapy
Snoezelen
Reminiscence therapy
269
Top 3 things leading to nursing home placement
Wandering
***Insomnia
Incontinence
270
Pathological anxiety
Excessive fear/anxiety response that is impairing or distressing rather than helpful or manageable
Occurs in context or with response to cues where there is no real threat
271
Having an anxiety disorder increased your risk of
Developing a chronic medical condition
272
Fear conditioning
273
Neurobiology of mood and anxiety disorders
The limbic system
The prefrontal cortex
274
Amygdala
Processes emotionally salient stimulant initiates the behavior response (accelerates fear response)
prefrontal cortex performs execute function, planning, decision making (shuts fear response down)
275
Hypothalamic-pituitary adrenal axis
Endocrine- slow response
Sympathetic nervous system- fast response
276
Fear extinction
Cognitive behavioral therapy
Graduated exposure
277
Main brain structure involved in fear and emotional processing
Amygdala
278
Diagnosis of a specific phobia
Fear/anxiety about object/situation
Persists for at least 6 months
279
Agoraphobia
Fear of being outside, around other people
Lasts more than 6 months
280
Clinical management of agoraphobia
Exposure therapy
281
Social anxiety disorder
Fear of social situations and scrutiny from others
Fear of acting in a way that will be humiliating or embarrassing
Lasts for at least 6 months
282
Generalized anxiety disorder
Excessive anxiety and worry for more than 6 months
Worry is difficult to control
283
Obsessive compulsive disorder
Presence of obsessions, compulsions or both
Obsessions-persistent thoughts
Compulsions- repetitive behaviors
284
Neurobiology of OCD
Cortico-striato-thalamo-cortical loop
285
What can cause the onset of OCD in children
PANDAS: loop for anti-streptolysin O tiger or DNase B antibodies
286
OCD management
Exposure and response prevention
SSRIs
Clomipramine
287
Management of anxiety disorders
SSRI
CBT
288
Adjustment disorder
Emotional or behavioral symptoms in response to identifiable stresses occurring within 3 months of onset of stressor
Symptoms are over within 6 moths characterized by depressed mood, anxious mood, mixed anxiety/depression, disturbance of conduct
289
PTSD
Severe trauma the constitutes a threat to the physical integration or life of the individual or another person
(Onset 1-3 months after trauma)
If <1 month it is acute stress disorder
290
Diagnostic criteria for PTSD
Exposure
Intrusion
Avoidance
Negative alterations in cognition or mood
Arousal and reactivity
Symptoms for more than a moths
Significant distress or impairment
291
PTSD can cause
Dissociative symptoms
Delayed expression
292
Acute stress disorder
3 days-1 moths after trauma exposure
293
PTSD treatment
SSRI Or SNRI
Psychotherapy (prolonged exposure therapy
294
Major depression vs demoralization
295
ODD
Angry
Defiant
Vindictiveness
Lasts at least 6 months
296
ODD is associate with
Distress
297
Conduct disorder
Aggression
Destruction
Deceitfulness
Serious violation of rules
Longer than 6 months
Lack of remorse or guilt
Callous-lack of empathy
Unconcearned about performance
Shallow or deficient affect
298
ODD and conduct disorder treatment
NO medication
Behavioral management training
299
ADHD
Neurodevelopmental disorder with core characteristics of behavior and response inhibition
Can be inattentive, hyperactive/impulse presentation, combined presentation
300
ADHD diagnostic criteria
Careless mistakes
Difficulty sustaining attention
Does not listen
Does not follow through
Difficulty organizing
Avoids tasks that require sustained mental effort
Loses things
Easily distracted
Often forgetful
Prior to age 12
Two or more settings
Reduced functioning
301
ADHD diagnosis
Clinical interview and history
Collateral information
302
Neuropsychological testing
Used for ADHD
Used to establish IQ, underlying learning disorders
303
Most common comorbidity of someone with ADHD
ODD
304
ADHD maturation delay
Right frontal side
305
ADHD treatment
Medication treatment (stimulants-amphetamines, methylphenidate) if active use disorder use atomoxetine
Behavioral therapy
306
Autism diagnosis
Deficits in social communication and interaction across multiple contexts
Restricted, repetitive patterns of behavior, interests, or activities
Must been in early development, cause impairment of functions
307
Autism specifiers
With or without intellectual impairment
With or without language impairment
308
Syndromes associated with autism
Fragile X
Tuberous sclerosis
Rett syndrome
309
Intellectual disability
Inherited- fragile X
Genetic- trisomy 21
Preventable- fetal alcohol disorder
310
Things that are not evidence based psychotherapy
311
Cognitive behavioral therapy has evidence for
Depression
Generalized anxiety disorder
Schizophrenia
ADHD
Bulima
Insomnia
312
Behavioral therapy has evidence for
ADHD
Obesity
Alcohol use disorder
Autism spectrum disorder
313
Parent management has evidence for
Disruptive behavior/ noncompliance
ODD
ADHD
314
Exposure therapy has strong evidence for
Specific phobias
OCD
Panic disorder
315
Prolonged exposure is
Modified for PTSD
316
When does therapy come first
Pediatric populations
Tics
Trichotillomania
Behavioral sleep disorders
Enuresis/encopresis
When a patient wants it
317
Piagets theory of cognitive development
318
Stages of cognitive development
319
Vygotsky sociocultural theory
Cognition is dependent on the social, cultural, and historical context
Culture defines what knowledge and skills a child needs to acquire and gives them the tools
The intermental constructs the intramental
All of this has to occur in zone of proximal development (what I can do with help)
320
Erik Eriksons psychological stages
Personality develops in predetermined order
Each stage has a crisis that must be resolved to move onto next stage
Failure to resolve a crisis results in stagnancy
321
Attachment theory
Stages:
Pre-attachment
Attachment in the making (3-6 months)
True (7-18 months)
assess using strange situation procedure
322
Strange situation response patterns
323
When are basic emotions developed
By 6 moths
324
When are complex emotions developed
18-24 months
325
Self concept evolution
326
Two general dimensions of parenting
Parental warmth and responsiveness
Parental control
327
Delirium
An acute mental disturbance caused by another medical condition characterized by confused thinking and disrupted attention
Disturbance in attention and awareness
Fluctuates throughout the day
Disturbance in cognition
Caused by another general medical condition
328
Delirium prevention and treatment
Re-orientation
Prevent dehydration and constipation
Access hypoxia
Encourage mobility
Medication review
Look for and treat medication
Treat pain
Good nutrition
Prevent sensory impairment
Avoid sleep disturbance
329
Medication treatment for delirium
No medications indicated
330
Testing for patients with delirium
331
Delirium risk factors
332
Delirium take home points
333
Somatic Symptoms Disorders are marked by
Cognitive distortions
“Being healthy means being symptom free”
“I have a symptom therefor it must be a disease”
Disproportionate and persistent thoughts about the seriousness of symptoms
Persistently high level of anxiety about health or symptoms
Excessive time and energy devoted to these concerns or health symptoms
334
Fictitious disorder
Falsification of symptoms associated with deception
Deception
Patient commonly causes symptoms
Inconsistent response to treatments
Common for people who wants attention
Seeking sick role and attention that comes with it
335
Functional Neurological Symptom disorder
Impaired coordination/balance
Paralysis/weakness
Inability to swallow
Loss of touch/pain
Blindness
Deafness
Mutism
Nonepileptic spells
336
Refeeding syndrome
Life threatening shifts of electrolytes that can be associated with anorexia
Must monitor phosphorous
337
Russells sign
Calluses on back of dominant hand associated with bulimia
338
Complications of bulimia
Esophageal rupture
339
Binge eating disorder
Binge eating without inappropriate compensatory behaviors
340
Personality disorder characteristics
Ego syntonic-limited insight
Don’t seek help
Do not have frank psychosis
341
What is a personality disorder
Enduring pattern that deviates marked
Pervasive and inflexible
Onset in adolescence
Stable over time
Leads to distress or impairment
342
Manifestations of personality disorders
Cognition
Emotional response
Interpersonal functioning
Impulse control
343
Cluster A personality disorders
Paranoid
Schizoid
Schizotypal
Odd and eccentric behaviors
344
Cluster B personality disorders
Antisocial
Borderline
Narcissistic
Histrionic
345
Cluster C personality disorders
Avoidant
Dependent
Obsessive-compulsive
346
Paranoid personality disorder
Mistrust in people
347
Schizoid personality disorder
Lifelong social withdrawal
348
Schizotypal personality disorder
Bizarre dress and speech
349
Narcissistic personality disorder
Heightened sense of self importance
Unempithetic, entitled
350
Histrionic Personality Disorder
Theatrical
Extroverted
Emotional
Sexually provocative
“Life of the party”
Connot maintain intimate relationships
351
Antisocial personality disorder
Refuses to confirm to social norms
No concearn for others
Does not learn from expense
Psychopath, sociopath
Continual criminal acts
Lacks a conscience
Cons others
Must have prior diagnosis of a conduct disorder before the age of 15
352
Borderline personality disorder
Erratic unstable behavior and mood
Borden
Feelings of aloneness
Impulsiveness
Suicide attempts
Mini psychotic episodes
353
Avoidant personality disorder
Timid
Sensitive to rejection
Socially withdrawn
Feelings of inferiority
Fearful of embarrassment and rejection
354
Dependent personality disorder
Get others to assume responsibility for their actions
Intense discomfort when being alone
Exaggerated fears of being helpless when alone
355
Obsessive compulsive personality disorder
Perfectionist
Orderly
Stubborn
Indecisive
Feelings of imperfection
356
OCPD
Limited insight
May think others cause their problems
Generally don’t seek help unless compelled by others
Ego dystonic
357
Personality disorder treatment
DBT
CBT
358
Psychosis
Symptom not diagnosis
Distorted perception of reality
Positive symptoms: Delusion, hallucinations/illusions, disorganized thinking/behavior
359
Delusions
Fixed false belief which is not in line with the beliefs of others in the patient’s culture
360
Perceptual disturbance
Hallucination: a sensory experience with no corresponding stimulus (auditory, visual, tactile, olfactory, gustatory)
361
Disorganized speech is indicative of
Disorganized thoughts
362
Negative symptoms of psychosis
Affective blunting- decreased emotional expression
Avolition- lack of motivation to engage in social activities
Apathy- lack of interest in engaging in social activities s
Anhedonia- lack of pleasure in activities
Alogia- decreased speech output, “poverty of speech”
363
Cognitive symptoms of psychosis
Problems with executive functioning
Deficits in working memory
Deficits in attention and focus
364
Criteria for schizophrenia
2 or more:
Delusions
Hallucinations
Disorganized speech
Grossly disorganized or catatonic behavior
Negative symptoms
Lasts more than 6 months
365
Brief psychotic disorder
One or more symptoms of schizophrenia
Lasting longer than 1 day but less than 1 moths
People return to premorbid level of function
366
Schizophreniform disorder
Meet criteria for schizophrenia except for the time requirement
Lasts longer than 1 month but less than 6 months
367
Schizoaffective disorder
368
Delusional disorder
369
Catatonia
370
Most effective treatment for schizophrenia
ECT
371
Dopamine blocking-related side effects
IMPORTANT
372
Bipolar disorder diagnosis s
Must have a manic episode
373
Bipolar disorder type 2
Recurrent depressive episodes and hypomanic episode
Must last at lease for days
374
Bipolar disorder type 1
At least one manic episode with recurrent depressive episodes
375
Environmental triggers for bipolar disorder
Sleep deprivation or disruption
Time changes
Season changes
Alcohol use
Drug use
Stress
376
Psychiatric emergency
Acute disturbance of thought, mood, behavior, or social relationship
Required immediate intervention
Has potential to rapidly become catastrophic outcome
Resources to handle situation are not currently available
377
Examples of psychiatric emergencies
Homicidal ideation
Auditory hallucinations commanding violence
Suicidal ideation
Underlying causes: substance intoxication/withdrawal, sever depression, psychosis, bipolar mania, antisocial personality disorder, adjustment disorder, personality disorder
378
Psychedelic
Used interchangeably with hallucinogen
Psilocybin
MDMA
Ketamine
THC
379
Psilocybin
Found in mushrooms
Increase self compassion, love, acceptance of death
Mystical experience
May cause hallucinations after withdrawal
380
MDMA
Releases supraphysiological levels of serotonin, dopamine, norepinephrine
Stimulates release of hormones like oxytocin
Enhance feelings of trust, openness, and connection to other people
Benefits more likely in conjunction with psychotherapy
May cause neurotoxicity
381
Ketamine
Used for treatment resistant depression (rapid reductions in suicidality)
NMDA receptor antagonism
382
CBD
Not related to misuse, abuse, or dependence
general anti-inflammatory and antioxidant properties
Used for chronic pain, mental health, psychosis, PTSD
383
Addiction
Treatable
Chronic medical disease involving complex interactions between brain circuits, genetics, the environment, and the individuals life experiences
Addictive behavior leads to compulsions and continued substance use despite harmful consequences
Prevention and treatment are generally successful
384
Substance use disorder criteria
A problematic pattern leading to clinically significant impairment or distress
385
Uppers substances
Stimulants
386
Downers substances
Alcohol
Sedative-hypnotic-anxiolytics
Opioids
Cannabis
387
Sideways substances
Hallucinogens
Dissociatives
388
Other substances
Nicotine/tabacco
Caffeine
Inhalants
Synthetic Cathinones
Steroids
389
Intoxication and withdrawal care
Supportive care
Monitor ABCs
Protect from self harm
Manage fluid/electrolyte balances
Symptomatic treatment
390
Stimulants
391
Downers
392
CIWA-Ar
Alcohol withdrawal state
393
Alcohol withdrawal treatment
Benzodiazepines
Anticonvulsants
Vitamin and electrolyte replacement
394
Wernicke encephalopathy’s
confusion, ataxia, ocular changes
IV thiamine followed by glucose
395
Korsakoff syndrome
Untreated wernicke
Chronic and irreversible
Anteriograde amnesia, confabulation, personality changes
396
Downers
397
Opioid overdose reversal
Naloxone
398
Opioid withdrawal
399
Downers
400
Cannabis use
401
Sideways
402
Stage 1 sleep (NREM1-N1)
Transition from wake to sleep
Hypnic jerks
Slow, rolling eye movements
403
Stage 2 sleep (NREM 2-N2)
Most common stage of sleep
No eye movement
Sleep spindles generated in thalamus
K-Complexes
404
Stage 3 sleep (NREM 3-N3)
Delta waves (0.5-2 Hz)
Dreaming can occur
Parasomnias
More during the first half of the night
405
REM sleep
More in latter half of the night
Relative paralysis
406
Sleep stage time length
90 minutes
407
the timing of _ is linked to body temp
REM
408
NREM accounts for _ of total sleep time
75-80%
409
Wakefulness
Coordinated activity of interconnected ascending arousal systems
410
Primary inhibitory neurotransmitter
GABA (sleep promoting)
Located in VLPO
411
Hypocretin (orexin)
Wake promoting (lateral and posterior hypothalamus)
Stabilizing neuromodulator
412
Wake activating neurotransmitters
Ach
Dopamine
Histamine
NE
Serotonin
413
Primary REM on neurotransmitter
Ach
414
Adenosine (sleep promoting) is inhibited by
Caffeine (adenosine receptor agonist)
415
Humanities context
Transdisciplinary
