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Neurocognitive Disorders Flashcards

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1
Q

What are neurocognitive disorders (NCDs)?

A

Comprise a group of conditions defined by a decline from previous level of cognitive functioning

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2
Q

What are the 6 cognitive domains that may be affected in neurocognitive disorders (NCDs)?

A

Complex attention

Executive function

Learning and memory

Language

Perceptual-motor skills

Social cognition (interaction)

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3
Q

What are the 3 main DSM-V categories of neurocognitive disorders (NCDs)?

A

Delirium

Mild NCDs

Major NCDs

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4
Q

What is delirium?

A

It is a medical emergency
- Think of it as an acute brain failure

May be the only early manifestation of serious illness

Reversible, but can potentially advance to coma, seizures, or death

Associated w/ high mortality
- Up to 40% of individuals die within 1 year of diagnosis

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5
Q

What is the ICU triad?

A

Delirium, pain, and agitation

All 3 of these interdependent conditions must be addressed

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6
Q

Epidemiology of delirium

A

50% of medically admitted patients develop delirium

Often goes unrecognized

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7
Q

Risk factors of delirium

A

Polypharmacy
- Including use of psychotropic medications (especially benzos and anticholinergics)

Advanced age

Preexisting cognitive impairment or depression

Prior history of delirium

Alcohol use

Severe or terminal illness

Multiple medical comorbidities

Impaired mobility

Hearing or vision impairment

Malnutrition

Male gender

Pain

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8
Q

What are the terms commonly used for delirium?

A

Toxic or metabolic encephalopathy

Acute organic brain syndrome

Acute confusional state

Acute toxic psychosis

ICU psychosis

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9
Q

Etiology of delirium

A

Almost any medical condition can cause delirium

DSM-V recognizes 5 broad categories:

  • Substance intoxication delirium
  • Substance withdrawal delirium
  • Medication-induced delirium
  • Delirium due to another medical condition
  • Delirium due to multiple etiologies
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10
Q

Common causes of medication-induced delirium

A
  • TCAs
  • Anticholinergics
  • Benzodiazepines
  • Non-benzodiazepine hypnotic (“Z-drugs”)
  • Corticosteroids
  • H2 blockers
  • Meperidine
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11
Q

Likely diagnosis and necessary testing of delirium + hemiparesis or other focal neurological signs/symptoms

A

CVA or mass lesion

Testing: head CT / brain MRI

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12
Q

Likely diagnosis and necessary testing of delirium + elevated blood pressure + papilledema

A

Hypertensive encephalopathy

Testing: head CT / brain MRI

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13
Q

Likely diagnosis and necessary testing of delirium + dilated pupils + tachycardia

A

Drug intoxication

Testing: urine toxicology screen

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14
Q

Likely diagnosis and necessary testing of delirium + fever + nuchal rigidity + photophobia

A

Meningitis

Testing: lumbar puncture

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15
Q

Likely diagnosis and necessary testing of delirium + tachycardia + tremor + thyromegaly

A

Thyrotoxicosis

Testing: free T4, T3, TSH

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16
Q

What are the most common precipitants of delirium in children?

A

Febrile illnesses

Medications

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17
Q

How does delirium generally manifest as on EEG?

A

Diffuse background slowing

Exception is delirium tremens:
- Associated w/ fast activity

EEG lacks sensitivity and specificity, but it is useful for ruling out non-convulsive seizures

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18
Q

Clinical manifestations of delirium

A

Primarily disorder of attention and awareness (i.e. orientation)

Cognitive deficits develop acutely over hours to days

Symptoms fluctuate throughout course of day, typically worsening at night

Other features:

  • Deficits in recent memory
  • Language abnormalities
  • Perceptual disturbances (usually visual - illusions / hallucinations)

Circadian rhythm disruption and emotional symptoms are common

Complete recover occurs in most hospitalized patients within about 1 week
- Some cognitive deficits can persist for months or remain indefinitely

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19
Q

What are the 3 types of delirium based on psychomotor activity?

A

MIXED TYPE:
- Pyschomotor activity may remain stable at baseline or fluctuate rapidly between hyperactivity and hypoactivity

HYPOACTIVE (“quiet”) TYPE:

  • Decreased psychomotor activity, ranging from drowsiness to lethargy to stupor
  • More likely to go undetected
  • More common in elderly

HYPERACTIVE TYPE (“ICU psychosis”)

  • Manifests w/ agitation, mood lability, and uncooperativeness
  • Less common, but more easily identified
  • More common in drug withdrawal / toxicity
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20
Q

What is the quick, first-glance bedside exam for suspected substance/mediation intoxication?

A

VALEUMS

  • Vital signs
  • Alertness level
  • Eyes (pupil size and position)
  • Urine (bladder distension, incontinence)
  • Mucous membranes (moisture)
  • Skin (temp and moisture)
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21
Q

If a patient presents w/ altered mental status, disorientation, confusion, agitation, or new-onset psychotic symptoms, what should you suspect?

A

Delirium!

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22
Q

What are the typical symptoms of delirium?

A

Short attention span

Disorientation

Fluctuations in level of consciousness

Visual hallucinations

Impairment in recent memory

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23
Q

DSM-V criteria of delirium

A

Disturbance in attention and awareness

Disturbance in an additional cognitive domain

Develops acutely over hours to days, represents a change from baseline, and tends to fluctuate

Not better accounted for by another neurocognitive disorder

Not occurring during a coma

Evidence from history, physical, or labs that the disturbance is direct consequence of another medical condition, substance intoxication / withdrawal, exposure to toxin, or due to multiple etiologies

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24
Q

Diagnosis of delirium

A

Confusion Assessment Method (CAM) is useful tool for evaluation of patient w/ suspected delirium:

  • Takes 5 mins to perform
  • Has high sensitivity and specificity
  • Diagnoses delirium in patient w/ inattention of acute onset and/or fluctuating course along w/ either disorganized thinking or altered consciousness

Inattention: distractibility or difficulty maintaining focus during evaluation

Disorganized thinking: derailment or loose associations

Level of consciousness: ranges from vigilant (hyperalert) to alert (normal) to lethargic (drowsy, but easily aroused) to stuporous (difficult to arouse) to comatose (unarousable to verbal stimulation)

Once delirium is diagnosed, the cause(s) should be sought

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25
Q

Workup of delirium to figure out cause

A

Finger-stick blood glucose, pulse-oximetry, arterial blood gases, ECG can quickly provide useful data at bedside

Labs obtained: basic metabolic panel, CBC w/ differential, urinalysis, and urine culture

Urine drug screen, blood alcohol level, therapeutic drug levels (e.g. antiepileptics, digoxin, lithium), hepatic panel, thyroid hormone levels, or CXR may be warranted depending on clinical presentation

Head imaging (head CT / brain MRI), EEG, and lumbar puncture should be performed if focal neurological deficits are present or cause of delirium can’t be identified w/ initial workup

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26
Q

Treatment of delirium

A

Treat underlying cause(s)

Address potential exacerbating factors

Encourage family member to stay at bedside to provide company and redirection as needed

Maintain adequate supervision, utilizing one-to-one sitter if necessary

Reorient patient on regular basis by drawing attention to time, place, and situation by keeping whiteboards, calendars, and clocks in plain sight

PHARMACOTHERAPY:
D2 antagonists (i.e. antipsychotics) are indicated if agitation puts patient or others at risk
- Haloperidol is preferred agent - can be administered orally, IM, or IV
- Can exacerbate EPS, so use w/ caution in patients w/ Parkinsonism

Benzodiazepines

  • Can cause, worsen, or prolong delirium
  • Do not use unless treating delirium due to alcohol or benzo withdrawal

Avoid the use of restraints (may worsen agitation and cause injury)

  • If restraints are necessary, use the least restrictive means appropriate for situation
  • Remove them as soon as patient meets criteria for release
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27
Q

Under what circumstances should you consider head CT for patient w/ delirium?

A

No underlying cause is evident on initial evaluation

Delirium occurs in context of head trauma

New focal neurological deficits detected on exam

Patient is unable / unwilling to cooperate w/ neurologic exam

No improvement occurs despite treatment of already identified causes

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28
Q

What medication should you avoid using in delirium?

A

Benzodiazepines, unless delirium is due to alcohol or benzo withdrawal
- These meds often worsen delirium by causing paradoxical disinhibition or oversedation

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29
Q

What characterizes non-delirium NCDs?

A

Characterized by more chronic cognitive decline that impacts functioning in daily activities

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30
Q

What characterizes mild NCDs?

A

Aka mild cognitive impairment

Experience difficulty w/ some of more complex activities of daily living, but are able to maintain their independence

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31
Q

What characterizes major NCDs?

A

Require assistance w/ independent activities of daily living (e.g. paying bills, managing meds, shopping for groceries)

Over time, the basic activities of daily living (e.g. feeding, toileting, bathing) are affected, eventually leading to total dependence

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32
Q

DSM-V criteria for mild and major NCDs

A

Both require functional decline in at least 1 cognitive domain relative to baseline as evidenced by:

  • Concern (expressed by patient or someone who knows them)
    • Mild NCDs: mild decline
    • Major NCDs: significant decline
  • Objective findings on cognitive testing (preferably standardized neuropsychological testing)
    • Mild: modest impairment
    • Major: substantial impairment
  • Effect on functioning in daily life
    • Mild: ability to perform; IADLs preserved
    • Major: impaired performance of IADLs / ADLs

Deficits do not occur exclusively in context of delirium

Deficits are not better explained by another mental disorder

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33
Q

Subcategories (by etiology) of mild and major NCDs

A

Dementias compromise large group of progressive and irreversible major NCDs that primarily affect elderly

Several other major NCDs present similarly to dementias, but their progression may be halted or even reversed w/ treatment:

  • Vitamin B12 deficiency
  • Thyroid dysfunction
  • Normal pressure hydrocephalus
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34
Q

Likely diagnosis and necessary testing of cognitive impairment w/ step-wise increase in severity + focal neurological signs

A

Vascular disease

Testing: head CT / brain MRI

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35
Q

Likely diagnosis and necessary testing of cognitive impairment + cogwheel rigidity + resting tremor

A

Lew body disease or Parkinson’s disease

Testing: clinical

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36
Q

Likely diagnosis and necessary testing of cognitive impairment + gait apraxia + urinary incontinence + dilated cerebral ventricles

A

Normal pressure hydrocephalus

Testing: head CT / brain MRI

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37
Q

Likely diagnosis and necessary testing of cognitive impairment + fatigue + cold intolerance + coarse hair + constipation

A

Hypothyroidism

Testing: TSH, free T4

38
Q

Likely diagnosis and necessary testing of cognitive impairment + paresthesias + diminished position and vibration sensation + megaloblasts on CBC

A

Vitamin B12 deficiency

Testing: Serum B12

39
Q

Likely diagnosis and necessary testing of cognitive impairment + tremor + Kayser-Fleischer rings + abnormal LFTs

A

Wilson’s disease

Testing: ceruloplasmin

40
Q

Likely diagnosis and necessary testing of cognitive impairment + diminished position and vibration sensation + Argyll Robertson pupils (Accommodation Response Present, response to light absent)

A

Neurosyphilis

Testing: CSF FTA-ABS and VDRL

41
Q

Diagnosis of mild and major NCDs

A

Asssessments:

  • MiniMental State Exam (MMSE):
    • Screening test used due to its speed and ease of administration
  • Mini-Cog
  • Blessed Orientation-Memory-Concentration (BOMC)
  • Montreal Cognitive Assessment (MoCA)
  • Frontal Assessment Battery (FAB)

Abnormal screening test indicates need for further testing, preferably formal neuropsychological testing

42
Q

Use of MMSE in the diagnosis of mild and major NCDs

A
  • Assesses orientation, attention / concentration, language, constrictional ability, and immediate and delayed recall

Sensitive for major NCDs (e.g. dementias)
- Perfect score: 30; Dysfunction <25

Not as sensitive for mild NCDs and early major NCDs
- Lacks specificity

Norm tables are available to adjust for age and education

43
Q

Use of Mini-Cog in the diagnosis of mild and major NCDs

A
  • Consists of 3-item recall and clock-drawing tasks

Positive screening for cognitive impairment:

  • No items recalled after 3 mins.
  • Only 1 or 2 items recalled w/ abnormal clock drawing

Negative screening:

  • All 3 times repeated correctly after 3 mins.
  • 1 or 2 items recalled w/ normal clock drawing
44
Q

What other symptoms are associated w/ the reversible cognitive impairment seen w/ thyroid dysfunction?

A

Hypothyroidism:
- Accompanied by fatigue and cold intolerance

Hyperthyroidism:
- In elderly may manifest as “apathetic thyrotoxicosis” = depression and lethargy

45
Q

What is on the MMSE?

A

Orientation (awareness):

  • Date
  • lace

Registration:
- Name 3 objects and repeat them

Attention:
- Serial 7s or spell “world” backwards

Recall (recent memory):
- Name 3 objects above 5 mins. later

Language:

  • Naming: pen, clock
  • Repetition: say ‘no ifs, ands, or buts’
  • Verbal comprehension (3-step command)
  • Written comprehension
  • Writing
  • Visuospatial skills: draw 2 intersecting pentagons

Total of 30 points

46
Q

What is Alzheimer’s disease (AD)?

A

Most common underlying etiology of major NCDs (dementias)

47
Q

Clinical manifestations of AD

A

Gradual progressive decline in cognitive functions

Primary cognitive domains affected:

  • Memory
  • Learning
  • Language

Personality changes, mood swings, and paranoia are very common

Motor and sensory symptoms are absent until late in course

On average, death occurs 10 years after diagnosis

48
Q

Diagnosis of AD

A

Definitive diagnosis can only be established postmortem
- Senile plaques and neurofibrillary tangles (also found in Down syndrome and even normal aging)

Diagnosis of possible NCD due to AD is made based on presence of clinical findings:

  • Insidious onset
  • Gradual progression
  • Impairment in 1 (mild NCD) or more (major NCD) cognitive domains

NCD due to AD is probable if there is evidence of causation by 1 of several single-gene variants

49
Q

What is the only way to definitively diagnose AD?

A

Postmortem pathological exam of brain

- Senile plaques and neurofibrillary tangles

50
Q

Etiology of AD

A

Accumulation of extraneuronal beta-amyloid plaques and intraneuronal tau protein tangles
- Associated w/ progressive brain atrophy

Approx. 1% of AD results from AD single-gene mutation (amyloid precursor protein, presenilin 1, or presenilin 2)
- Results in early onset of symptoms

Having epsilon-4 variant of apolipoprotein gene is risk factor for developing early-onset AD

51
Q

Epidemiology of AD

A

AD pathology is estimated to play role in 60-90% of major NCDs

Approx. 50% of patients w/ AD pathology actually have NCD due to multiple etiologies

2/3 of patients diagnosed w/ AD are women

Diagnosed after age 65 in vast majority of individuals

52
Q

Adults w/ what disorder has an increased risk of developing AD in midlife?

A

Adults w/ Down syndrome

53
Q

Treatment of AD

A

No cure / truly effective treatment

Multidisciplinary approach is necessary

Any treatment plan must include caregiver support

Supportive care via behavioral, social, and environmental interventions

PHARMACOTHERAPY:
Cholinesterase inhibitors (e.g. donepezil, rivastigmine, galantamine)
- May slow clinical deterioration by 6-12 months in up to 50% of patients w/ mild-to-mod AD

NMDA receptor antagonist (memantine)
- May provide modest benefit in patients w/ mod-to-severe disease

Antipsychotic meds

  • Often used to treat agitation and aggression
  • Low doses should be prescribed for short periods of time because they are associated w/ increased mortality in patients w/ dementia
  • Informed consent should be obtained from patients and/or designated decision makers
  • Monitor closely for side effects
54
Q

What is the black box warning of antipsychotics in regards to dementia?

A

Increased risk of death in patients w/ dementia

55
Q

What is vascular disease causing NCD (vascular cognitive impairment)?

A

2nd most common single cause of major NCD after AD
- Account for approx. 20% of major NCDs

Evidence of vascular disease is found in 1/2 of all major NCDs
- Most commonly comorbid w/ AD pathology (NCD due to multiple etiologies)

Cognitive decline occurs as result of at least 1 of the following mechanisms:

  • Large vessel strokes (usually cortical)
  • Small vessel strokes (lacunar infarcts)
  • Microvascular disease affecting periventricular white matter

Effects vary based on size, location, and number of infarcts

56
Q

Risk factors for vascular disease (vascular cognitive impairment)

A
  • Hypertension
  • Diabetes
  • Smoking
  • Obesity
  • Hyperlipidemia
  • Atrial fibrillation
  • Old age
57
Q

What can a lesion to the frontal lobe manifest as?

A

Spectrum of symptoms including:

  • Personality changes
  • Disinhibition
  • Inappropriate behavior
  • Aggression
  • Apathy
  • Amotivation
  • Paranoia
58
Q

Clinical manifestations of vascular disease causing NCD (vascular cognitive impairment)

A

Presentation and progression of cognitive impairment are variable:

  • Classically demonstrates step-wise deterioration (correspond w/ occurrence of micro-infarcts)
  • May present w/ acute onset followed by partial improvement
  • May have insidious onset w/ gradual decline similar to AD

Complex attention and executive functions are cognitive domains typically affected in small vessel disease

Confirmation of diagnosis requires neuroimaging w/ findings that correlate to clinical picture

59
Q

Treatment of vascular disease causing NCD (vascular cognitive impairment)

A

No cure or truly effective treatment

Manage risk factors w/ goal of preventing future strokes

Symptomatic treatment is similar to DA

60
Q

What is lewy body disease (LBD)?

A

Major pathologic features of LBD are:

  • Lewy bodies (pathologic aggregations of alpha-synuclein)
  • Lewy neuritesin brain (primarily in basal ganglia)
61
Q

Clinical manifestations of LBD

A

Progressive cognitive decline

Core features:

  • Waxing and waning of cognition, especially in areas of attention and alertness
  • Visual hallucinations (vivid, colorful, well-formed images of animals or small people)
  • Development of extrapyramidal signs (Parkinsonism) at least 1 year after cognitive decline becomes evident

Suggestive features:

  • Rapid eye movement (REM) sleep behavior disorder (violent movement during sleep in response to dreams - often fighting)
  • Pronounced antipsychotic sensitivity

Commonly coexists w/ AD and/or cerebrovascular disease as NCD due to multiple etiologies

62
Q

Diagnosis of LBD

A

Definitive diagnosis can only be made w/ autopsy

Possible NCD w/ Lewy bodies:
- Only 1 core feature or >= 1 suggestive feature

Probable NCD w/ Lewy bodies:
- >=2 core features OR 1 core feature and >= 1 suggestive feature

63
Q

Treatment of LBD

A

PHARMACOTHERAPY:
Cholinesterase inhibitors
- For cognitive and behavioral symptoms

Quetiapine or clozapine

  • For psychotic symptoms
  • Use lowest effective dose for shortest period of time possible
  • Monitor closely for adverse effects (EPS, sedation, increased confusion, autonomic dysfunction, signs of NMS)

Levodopa-carbidopa

  • For Parkinsonism
  • Not as effective a in idiopathic Parkinson’s disease
  • May exacerbate psychosis or REM sleep behavior disorder

Melatonin and/or clonazepam
- For REM sleep behavior disorder

64
Q

What is frontotemporal degeneration (FTD)?

A

Includes diverse group of clinical and pathological disorders that typically present between ages 45 and 65

Approx. 40% are familial and 10% are AD

65
Q

Clinical manifestations of FTD

A

Cognitive deficits in:

  • Attention
  • Abstraction
  • Planning
  • Problem solving

Behavioral variant:

  • Disinhibited verbal, physical, or sexual behavior
  • Overeating or oral exploration of inanimate objects
  • Lack of emotional warmth, empathy, or sympathy
  • Apathy or inertia
  • Preservation, repetitive speech, rituals, or obsessions
  • Decline in social cognition and/or executive abilities
Language variant (primary progressive aphasia):
- Difficulties w/ speech and comprehension

Relative sparing of learning / memory and perceptual-motor function

Many individuals have features of both behavioral and language variants

Increased sensitivity to adverse effects of antipsychotics

66
Q

Pathology of FTD

A

Marked atrophy of frontal and temporal lobes

67
Q

Diagnosis of FTD

A

Definitive diagnosis can’t be made until autopsy

FTD is probable if:

  • Frontotemporal atrophy is evident on structural imaging
  • Hypoactivity is visualized on functional imaging in context of characteristic clinical signs
68
Q

Treatment of FTD

A

Symptom-focused

PHARMACOTHERAPY:
Serotonergic meds (e.g. SSRIs, trazodone)
- May help reduce disinhibition, anxiety, impulsivity, repetitive behaviors, and eating disorders

69
Q

What is HIV infection in regards to NCD?

A

Most common infectious agent known to cause cognitive impairment

25% of persons infected w/ HIV meet mild NCD criteria

<5% meet major NCD criteria

70
Q

Risk factors of HIV infection causing NCD

A
  • History of severe immunosuppression
  • High viral loads in CSF
  • Advanced HIV infection
71
Q

Clinical manifestations of HIV infection causing NCD

A

Variable presentation depending on part(s) of brain affected

Decline may be observed in:

  • Executive functioning
  • Attention
  • Working memory
  • Psychomotor activity

Psychiatric and neuromotor symptoms may also be present

72
Q

Diagnosis of HIV infection causing NCD

A

Mild or major NCD attributable to confirmed HIV infection

73
Q

Treatment of HIV infection causing NCD

A

PHARMACOTHERAPY:
Highly active antiretroviral therapy (HAART)
- Improves cognition in some patients

Psychostimulants
- Target fatigue, apathy, and psychomotor retardation

74
Q

What is Huntington’s disease (HD)?

A

Genetic disorder resulting from trinucleotide (CAG) repeats in gene encoding huntingtin (HTT) protein on chromosome 4

AD mode of inheritance

75
Q

Clinical manifestations of HD

A

Characterized by triad of:

  • Motor
  • Cognitive
  • Psychiatric symptoms (depression, apathy, irritability, obsessions, impulsivity)

Average age at diagnosis is 40 years

Cognitive decline and behavioral changes can precede onset of motor signs by up to 15 years

Executive function is primary cognitive domain affected

Patients are often aware of deteriorating mentation
- Increased rate of suicide

Movement disorders include:

  • Chorea (jerky, dance-like movements)
  • Bradykinesia
76
Q

Diagnosis of HD

A

Extrapyramidal movement disorder in individual w/ either family history of HD or genetic testing that confirms increased # of CAG repeats in HTT gene

Mild/major NCD due to HD may be diagnosed prior to onset of motor signs if individual is determined to be at risk based on family history or genetic testing

77
Q

Treatment of HD

A

Symptom-directed therapy

PHARMACOTHERAPY:
Tetrabenazine
Atypical (second-generation) antipsychotics

78
Q

What is Parkinson’s disease (PD)?

A

Idiopathic, progressive neurodegenerative disease

Characterized by depletion of dopamine in basal ganglia

Up to 75% of patients w/ PD meet criteria for major NCD typically late in course of disease

79
Q

Clinical manifestations of PD

A

Motor signs:

  • Rigidity
  • Resting tumor
  • Bradykinesia
  • Postural instability

Cognitive manifestations:

  • Executive dysfunction
  • Visuospatial impairments

Depression, anxiety, personality changes, and apathy are common

Psychotic symptoms:

  • Visual hallucinations
  • Paranoid delusions
  • May result from disease itself or as adverse effects of meds
80
Q

Diagnosis of PD

A

Diagnosis requires presence of bradykinesia and either tremor or rigidity

Asymmetry of motor symptoms and favorable response to dopaminergic therapy support diagnosis

Mild/major NCD attributed to PD if cognitive decline appears after onset of motor symptoms and no other underlying etiology is identified

81
Q

Treatment of PD

A

PHARMACOTHERAPY:
Motor symptoms are most commonly treated w/ carbidopa-levodopa and/or dopamine agonists

Cholinesterase inhibitors

  • Used to target cognitive symptoms
  • May ameliorate some of neuropsychiatric symptoms (hallucinations)

Psychotic symptoms may respond to reduction in dose of dopamine agonists

Quetiapine and clozapine

  • Preferred meds for treatment of psychotic symptoms that are not responsive to dose reduction
  • Other antipsychotics should be avoided as they tend to exacerbate motor symptoms of PD
82
Q

What pharmacotherapy can exacerbate motor symptoms of PD?

A

Antipsychotic meds

83
Q

What is prion disease?

A

Form of subacute spongiform encephalopathy caused by proteinaceous infectious particles (prions)

Most cases occur sporadically

Most common type is Creutzfeldt-Jakob disease

Up to 15% are familial (AD)

<1% are iatrogenic

84
Q

Clinical manifestations of prion disease

A

Insidious onset w/ rapidly progressive cognitive decline

Difficulties w/ concentration, memory, and judgment occur early

> 90% of patients experience myoclonus (often provoked by startle) at some point in illness

Depression, apathy, and hypersomnia are common

Basal ganglia and cerebellar dysfunction are present in majority of individuals and present as:

  • Ataxia
  • Nystagmus
  • Hypokinesia
85
Q

Diagnosis of prion disease

A

Definitive diagnosis requires analysis of brain tissue obtained via biopsy or autopsy

Diagnosis of probable CJD requires:

  • Rapid progression of cognitive decline
  • At least 2 of the following typical features:
    1. Myoclonus
    2. Visual or cerebellar signs
    3. Pyramidal or extrapyramidal signs
    4. Akinetic mutism
  • Supportive findings from at least 1 diagnostic modality:
    1. Periodic sharp wave complexes on EEG
    2. CSF positive for 14-3-3 proteins
    3. Lesions in putamen or caudate nucleus on MRI
86
Q

Treatment of prion disease

A

No effective treatment exists

Most individuals die within 1 year of diagnosis

87
Q

What is rapidly progressive cognitive decline w/ myoclonus suggestive of?

A

Creutzfeldt-Jakob disease

88
Q

What is normal pressure hydrocephalus (NPH)?

A

Potentially reversible cause of cognitive dysfunction

Enlarged ventricles (on imaging) w/ localized elevation of CSF pressure, but normal opening pressures on LP

Etiology is either idiopathic or secondary to obstruction of CSF reabsorption sites due to infection (meningitis) or hemorrhage (subarachnoid or intraventricular)

89
Q

Clinical manifestations of NPH

A 
THE 3 Ws OF NPH:
Wobbly (gait disturbance)
- Most likely to be the first manifestation 
- Slow w/ short steps
- Broad-based w/ outwardly rotated feet
- Feet appear to be stuck to floor 
- Postural instability leads to recurrent falls
- Most responsive to treatment

Wet (urinary incontinence)

  • May begin as urinary urgency
  • Gait disturbance interferes w/ reaching toilet before loss of urine
  • In later stages, apathy may contribute

Wacky (cognitive impairment)

  • Insidious onset
  • Executive dysfunction
  • Psychomotor retardation
  • Decreased attention
  • Apathy
90
Q

Diagnosis of NPH

A

Clinical manifestations: wacky (cognitive impairment), wobbly (gait disturbance), and wet (urinary incontinence)

Neuroimaging shows enlargement of ventricles out of proportion to cortical atrophy

Clinical improvement w/ CSF removal via lumbar puncture is supportive of diagnosis

91
Q

Treatment of NPH

A

Placement of shunt (usually ventriculoperitoneal or VP) may improve symtpoms

Of the clinical triad, the cognitive impairment is least likely to improve

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