Neurocognitive Disorders Flashcards
What are neurocognitive disorders (NCDs)?
Comprise a group of conditions defined by a decline from previous level of cognitive functioning
What are the 6 cognitive domains that may be affected in neurocognitive disorders (NCDs)?
Complex attention
Executive function
Learning and memory
Language
Perceptual-motor skills
Social cognition (interaction)
What are the 3 main DSM-V categories of neurocognitive disorders (NCDs)?
Delirium
Mild NCDs
Major NCDs
What is delirium?
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
What is the ICU triad?
Delirium, pain, and agitation
All 3 of these interdependent conditions must be addressed
Epidemiology of delirium
50% of medically admitted patients develop delirium
Often goes unrecognized
Risk factors of delirium
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
What are the terms commonly used for delirium?
Toxic or metabolic encephalopathy
Acute organic brain syndrome
Acute confusional state
Acute toxic psychosis
ICU psychosis
Etiology of delirium
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
Common causes of medication-induced delirium
- TCAs
- Anticholinergics
- Benzodiazepines
- Non-benzodiazepine hypnotic (“Z-drugs”)
- Corticosteroids
- H2 blockers
- Meperidine
Likely diagnosis and necessary testing of delirium + hemiparesis or other focal neurological signs/symptoms
CVA or mass lesion
Testing: head CT / brain MRI
Likely diagnosis and necessary testing of delirium + elevated blood pressure + papilledema
Hypertensive encephalopathy
Testing: head CT / brain MRI
Likely diagnosis and necessary testing of delirium + dilated pupils + tachycardia
Drug intoxication
Testing: urine toxicology screen
Likely diagnosis and necessary testing of delirium + fever + nuchal rigidity + photophobia
Meningitis
Testing: lumbar puncture
Likely diagnosis and necessary testing of delirium + tachycardia + tremor + thyromegaly
Thyrotoxicosis
Testing: free T4, T3, TSH
What are the most common precipitants of delirium in children?
Febrile illnesses
Medications
How does delirium generally manifest as on EEG?
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
Clinical manifestations of delirium
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
What are the 3 types of delirium based on psychomotor activity?
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
What is the quick, first-glance bedside exam for suspected substance/mediation intoxication?
VALEUMS
- Vital signs
- Alertness level
- Eyes (pupil size and position)
- Urine (bladder distension, incontinence)
- Mucous membranes (moisture)
- Skin (temp and moisture)
If a patient presents w/ altered mental status, disorientation, confusion, agitation, or new-onset psychotic symptoms, what should you suspect?
Delirium!
What are the typical symptoms of delirium?
Short attention span
Disorientation
Fluctuations in level of consciousness
Visual hallucinations
Impairment in recent memory
DSM-V criteria of delirium
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
Diagnosis of delirium
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
Workup of delirium to figure out cause
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
Treatment of delirium
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
Under what circumstances should you consider head CT for patient w/ delirium?
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
What medication should you avoid using in delirium?
Benzodiazepines, unless delirium is due to alcohol or benzo withdrawal
- These meds often worsen delirium by causing paradoxical disinhibition or oversedation
What characterizes non-delirium NCDs?
Characterized by more chronic cognitive decline that impacts functioning in daily activities
What characterizes mild NCDs?
Aka mild cognitive impairment
Experience difficulty w/ some of more complex activities of daily living, but are able to maintain their independence
What characterizes major NCDs?
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
DSM-V criteria for mild and major NCDs
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
Subcategories (by etiology) of mild and major NCDs
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
Likely diagnosis and necessary testing of cognitive impairment w/ step-wise increase in severity + focal neurological signs
Vascular disease
Testing: head CT / brain MRI
Likely diagnosis and necessary testing of cognitive impairment + cogwheel rigidity + resting tremor
Lew body disease or Parkinson’s disease
Testing: clinical
Likely diagnosis and necessary testing of cognitive impairment + gait apraxia + urinary incontinence + dilated cerebral ventricles
Normal pressure hydrocephalus
Testing: head CT / brain MRI
Likely diagnosis and necessary testing of cognitive impairment + fatigue + cold intolerance + coarse hair + constipation
Hypothyroidism
Testing: TSH, free T4
Likely diagnosis and necessary testing of cognitive impairment + paresthesias + diminished position and vibration sensation + megaloblasts on CBC
Vitamin B12 deficiency
Testing: Serum B12
Likely diagnosis and necessary testing of cognitive impairment + tremor + Kayser-Fleischer rings + abnormal LFTs
Wilson’s disease
Testing: ceruloplasmin
Likely diagnosis and necessary testing of cognitive impairment + diminished position and vibration sensation + Argyll Robertson pupils (Accommodation Response Present, response to light absent)
Neurosyphilis
Testing: CSF FTA-ABS and VDRL
Diagnosis of mild and major NCDs
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
Use of MMSE in the diagnosis of mild and major NCDs
- 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
Use of Mini-Cog in the diagnosis of mild and major NCDs
- 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
What other symptoms are associated w/ the reversible cognitive impairment seen w/ thyroid dysfunction?
Hypothyroidism:
- Accompanied by fatigue and cold intolerance
Hyperthyroidism:
- In elderly may manifest as “apathetic thyrotoxicosis” = depression and lethargy
What is on the MMSE?
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
What is Alzheimer’s disease (AD)?
Most common underlying etiology of major NCDs (dementias)
Clinical manifestations of AD
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
Diagnosis of AD
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
What is the only way to definitively diagnose AD?
Postmortem pathological exam of brain
- Senile plaques and neurofibrillary tangles
Etiology of AD
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
Epidemiology of AD
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
Adults w/ what disorder has an increased risk of developing AD in midlife?
Adults w/ Down syndrome
Treatment of AD
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
What is the black box warning of antipsychotics in regards to dementia?
Increased risk of death in patients w/ dementia
What is vascular disease causing NCD (vascular cognitive impairment)?
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
Risk factors for vascular disease (vascular cognitive impairment)
- Hypertension
- Diabetes
- Smoking
- Obesity
- Hyperlipidemia
- Atrial fibrillation
- Old age
What can a lesion to the frontal lobe manifest as?
Spectrum of symptoms including:
- Personality changes
- Disinhibition
- Inappropriate behavior
- Aggression
- Apathy
- Amotivation
- Paranoia
Clinical manifestations of vascular disease causing NCD (vascular cognitive impairment)
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
Treatment of vascular disease causing NCD (vascular cognitive impairment)
No cure or truly effective treatment
Manage risk factors w/ goal of preventing future strokes
Symptomatic treatment is similar to DA
What is lewy body disease (LBD)?
Major pathologic features of LBD are:
- Lewy bodies (pathologic aggregations of alpha-synuclein)
- Lewy neuritesin brain (primarily in basal ganglia)
Clinical manifestations of LBD
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
Diagnosis of LBD
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
Treatment of LBD
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
What is frontotemporal degeneration (FTD)?
Includes diverse group of clinical and pathological disorders that typically present between ages 45 and 65
Approx. 40% are familial and 10% are AD
Clinical manifestations of FTD
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
Pathology of FTD
Marked atrophy of frontal and temporal lobes
Diagnosis of FTD
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
Treatment of FTD
Symptom-focused
PHARMACOTHERAPY:
Serotonergic meds (e.g. SSRIs, trazodone)
- May help reduce disinhibition, anxiety, impulsivity, repetitive behaviors, and eating disorders
What is HIV infection in regards to NCD?
Most common infectious agent known to cause cognitive impairment
25% of persons infected w/ HIV meet mild NCD criteria
<5% meet major NCD criteria
Risk factors of HIV infection causing NCD
- History of severe immunosuppression
- High viral loads in CSF
- Advanced HIV infection
Clinical manifestations of HIV infection causing NCD
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
Diagnosis of HIV infection causing NCD
Mild or major NCD attributable to confirmed HIV infection
Treatment of HIV infection causing NCD
PHARMACOTHERAPY:
Highly active antiretroviral therapy (HAART)
- Improves cognition in some patients
Psychostimulants
- Target fatigue, apathy, and psychomotor retardation
What is Huntington’s disease (HD)?
Genetic disorder resulting from trinucleotide (CAG) repeats in gene encoding huntingtin (HTT) protein on chromosome 4
AD mode of inheritance
Clinical manifestations of HD
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
Diagnosis of HD
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
Treatment of HD
Symptom-directed therapy
PHARMACOTHERAPY:
Tetrabenazine
Atypical (second-generation) antipsychotics
What is Parkinson’s disease (PD)?
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
Clinical manifestations of PD
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
Diagnosis of PD
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
Treatment of PD
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
What pharmacotherapy can exacerbate motor symptoms of PD?
Antipsychotic meds
What is prion disease?
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
Clinical manifestations of prion disease
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
Diagnosis of prion disease
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
Treatment of prion disease
No effective treatment exists
Most individuals die within 1 year of diagnosis
What is rapidly progressive cognitive decline w/ myoclonus suggestive of?
Creutzfeldt-Jakob disease
What is normal pressure hydrocephalus (NPH)?
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)
Clinical manifestations of NPH
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
Diagnosis of NPH
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
Treatment of NPH
Placement of shunt (usually ventriculoperitoneal or VP) may improve symtpoms
Of the clinical triad, the cognitive impairment is least likely to improve
