Central Nervous System Degenerative Disorders
Delirium/Dementia
I. Definitions
Confusional state—characterized by inability to think with proper speed, clarity, and coherence and associated with disorientation, decreased attention and concentration, impaired immediate recall, and diminution of all mental activity.
Delirium—an acute confusional state marked by prominent alterations in perception and consciousness and associated with vivid hallucinations, delusions, heightened alertness and agitation, hyperactivity of psychomotor and autonomic functions, insomnia, a tendency to convulse, and intense emotional disturbances.
Dementia—syndrome characterized by a deterioration of function in multiple cognitive/intellectual areas in an individual who had previously possessed a “normal” mind with little or no disturbance of perception or consciousness.
II. Characteristics of Delirium (think delirium tremens)
Symptoms develop over 2 to 3 days.
Initial signs/symptoms
Decreased concentration, irritability, tremulousness, insomnia, poor appetite
Convulsions (perhaps a “flurry”—30% of cases)
Dreams (unpleasant and vivid)
Disorientation (transient illusions and hallucinations)
Later signs/symptoms
Clouding of sensorium/inattention
Paranoia
Altered perception
Tremor
Insomnia
Autonomic hyperactivity
Duration of 2 days to a few weeks
Recovery is usually complete. Heralded by increased lucid intervals and sound sleep.
Continuum of severity from patient to patient
III. Causes of Delirium
Intoxication
Drugs
Alcohol
Anticholinergics
Sedative hypnotics
Opiates
Digitalis derivatives
Steroids
Salicylates
Antibiotics
Anticonvulsants
Antiarrhythmics
Antihypertensives
H2 blockers
Antineoplastics
Lithium
Antiparkinsonians
Disulfiram
Indomethacin
Cocaine
Glutethimide
Antipsychotics
Meprobamate
Phencyclidine hydrochloride (PCP)
Antidepressants
Others
Inhalants
Gasoline
Glue
Ether
Nitrous oxide
Nitrates
Toxins
Industrial
Carbon disulfide
Organic solvents
Bromide
Methyl chloride
Heavy metals
Organophosphates
Carbon monoxide
Plants and mushrooms
Venom
Withdrawal syndromes
Alcohol
Sedatives/hypnotics
Amphetamines
Metabolic disorders
Hypoxia
Hypoglycemia
Hepatic, pulmonary, renal, pancreatic insufficiency
Errors of metabolism
Porphyria
Carcinoid
Wilson disease
Nutritional disorders
Vitamin deficiencies
B12
Nicotinic acid
Thiamine
Folate
Pyridoxine
Hypervitaminosis—vitamin A and D intoxication
Fluid/electrolyte disorders
Dehydration or water intoxication
Alkalosis/acidosis
Excesses or deficiencies of Na, Ca, Mg, and so forth
Hormonal disorders
Hyperthyroidism/hypothyroidism
Hyperinsulinism
Hypopituitarism
Addison disease
Cushing syndrome
Hypoparathyroidism/hyperparathyroidism
Infection
Systemic—most anything, especially pneumonia and urinary tract infection in older patients; also typhoid, septicemia, rheumatic fever
Intracranial (acute, subacute, chronic)
Viral encephalitis
Aseptic meningitis
Herpes
Rabies
Fungal meningitis
Bacterial meningitis
Neoplasms
Metastases or meningeal carcinomatosis
Paraneoplastic (limbic encephalitis)
Primary tumors of temporal lobe, parietal lobe, and brainstem
Inflammatory—central nervous system (CNS) vasculitis
Trauma
Subarachnoid hemorrhage
Postconcussive delirium
Cerebral contusions or lacerations
Miscellaneous
Postconvulsive
Postoperative/intensive care unit
Mixed
Poststroke
IV. Evaluation
History and physical examination
Query family.
Get good time course.
Look for evidence of systemic disease, intoxication, seizure, etc.
Conduct good mental status examination
Computed tomography (CT) scan (usually without contrast)
Chest radiograph
Electrocardiogram
Urinalysis and urine drug screen
Serum ethanol level
Areterial blood gas
Serum for the following: complete blood count (CBC), Chem 18 (with electrolytes and liver function tests [LFTs]), amylase, B12, folate, thyroid function tests, rapid plasma regain, ± blood cultures (if febrile), erythrocyte sedimentation rate, antinuclear antibody, rheumatoid factor; consider obtaining HIV antibody titer and cardiac enzymes
Electroencephalogram (EEG): may show nonfocal slow activity (5 to 7 Hz); may show fast activity or may be normal; triphasic waves may be present
Lumbar puncture
V. Management
Control underlying medical illness.
Place patient in quiet environment with dim light.
Protect patient against injury.
Discontinue possible causative/exacerbating drugs and limit sedation (except in withdrawal states).
Administer intravenous fluid, thiamine, multivitamins, folate, and glucose after thiamine given.
Frequent vitals
VI. Characteristics of Dementia
Conventionally said to involve impairment in memory and one other cognitive sphere (e.g., language, praxis, calculation, judgment, visuospatial orientation, abstract thinking, concentration)
May have behavioral abnormalities and personality changes
Little or no disturbance of consciousness or perception (delirium must be absent)
Definition does not imply a specific cause, progressive course, or irreversibility.
Subcortical dementia
Characterized by forgetfulness, slowed mentation, apathy, depression, psychomotor retardation, perhaps a disorder of movement, and so forth.
Relative sparing of “cortical” functions (e.g., memory, language, praxis, naming, calculation)
Prototype: AIDS dementia complex, Huntington disease
Predominant pathologic finding is usually in basal ganglia and thalamus, although no form of dementia is strictly cortical or subcortical.
VII. Relative Frequency of Types
Alzheimer disease—60%
Alzheimer disease + other disorders—10%
Vascular disease—5%
Other degenerative diseases—5%
Treatable causes (e.g., tumor, ethanol-alcohol)—10%
Reversible dementia (i.e., depression, drugs, metabolic)—5%
Miscellaneous—5%
VIII. Causes of Dementia
Neurodegenerative
AD
Dementia with Lewy bodies
Pick disease and other frontotemporal dementias
Huntington disease
Progressive supranuclear palsy
Parkinson disease, Shy-Drager syndrome
Olivopontocerebellar atrophy
Familial dementia with spastic paraparesis
Parkinson-amyotrophic lateral sclerosis (ALS) dementia complex of Guam
Cerebro-cerebellar or cerebrobasal ganglionic degenerations
Progressive hemiatrophy
Vascular
Multi-infarct (including Binswanger disease) and bilateral cortical infarcts or unilateral cortical infarcts in eloquent areas
Hypoperfusion following cardiac arrest
Structural/traumatic
Hydrocephalus—communicating or non-communicating
Chronic subdural hematoma
Brain tumor
Midbrain hemorrhage
Cerebral contusion
Postradiation
Brain abscess
Metabolic/nutritional/endocrine/toxic
Hypothyroidism
Cushing syndrome
Wernicke-Korsakoff syndrome (thiamine deficiency)
Subacute combined degeneration (vitamin B12 deficiency)
Pellagra—nicotinic acid deficiency
Wilson disease
Hepatic encephalopathy
Porphyria
Uremia
Electrolyte disorders (e.g., hypercalcemia)
Thiamine deficiency
Chronic drug intoxication
Chronic heavy metal toxicity (e.g., lead)
Carbon monoxide poisoning (chronic)
Infections
HIV-associated dementia
Neurosyphilis
Subacute sclerosing panencephalitis
Progressive multifocal leukoencephalopathy
Whipple disease
Cryptococcosis
Postviral encephalitic states
Chronic fungal or tuberculous meningitis
Disorders of myelin
Multiple sclerosis
Marchiafava-Bignami disease
Leukodystrophies (see section H, “Inherited Neurometabolic Disorders”)
Neoplastic
Meningeal carcinomatosis
Limbic encephalitis
Inherited neurometabolic disorders
Leukodystrophies (such as Krabbe disease, metachromatic, adrenoleukodystrophy)
Lipid storage diseases (such as Tay-Sach disease, Niemann Pick disease)
Myoclonic epilepsy (neuronal ceroid lipofuscinosis)
Epilepsy
Depression—pseudodementia
Collagen-Vascular/Inflammatory
Sjögren syndrome
Systemic lupus erythrematosus
Neurosarcoidosis, and so forth
Miscellaneous (Prion diseases)
Creutzfeldt-Jakob disease (sporadic, iatrogenic, new variant, and familial types)
Gerstmann-Straussler-Scheinker disease
Fatal familial and fatal sporadic insomnia
Note: Remember the mnemonic for causes of dementia: DEMENTIA
D—degenerative, depression, drugs
E—endocrine
M—metabolic, myelin
E—epilepsy
N—neoplasm, nutrition
T—toxic, trauma
I—infection, inflammation, inherited disorders, infarction
A—atherosclerotic/vascular
S—structural, systemic
IX. Dementia and Delirium Quick Reference Table
Feature | Cortical Dementia | Subcortical Dementia | Delirium |
|---|---|---|---|
Onset | Insidious | Insidious | Sudden |
Duration | Months to years | Months to years | Hours to days |
Course | Progressive | Progressive | Fluctuating |
Attention | Normal | Normal | Fluctuating |
Speech | Normal | Hypophonic, dysarthric | Slurred, incoherent |
Language | Aphasic | Normal or anomic | Anomia, dysgraphia |
Memory | Learning deficit (AD) | Retrieval deficit | Encoding deficit |
Cognition | Acalculia, concrete | Slow, dilapidated | Impaired |
Awareness | Impaired | Preserved | Impaired |
Demeanor | Disinhibited | Apathetic | Apathetic, agitated |
Psychosis | Possible | Possible | Often florid |
Motor signs | None | Tremor, dystonia | Tremor, asterixis |
EEG | Diffuse slowing | Normal or mild slowing | Moderate-to-severe slowing |
AD, Alzheimer’s disease | |||
X. Dementia Deficits Table
AD | PD | HD | PSP | ||
|---|---|---|---|---|---|
Orientation | I | N | N | N | |
Memory | |||||
Immediate | I | I | I | N | |
Delayed | SI | I | I | N | |
Recognition | SI | N | N | N | |
% Retained | <50 | 50-80 | 50-80 | 50-80 | |
Executive function | SI | SI | SI | SI | |
Language | |||||
Naming | SI | N | N | N | |
Fluency | I | SI | SI | SI | |
Visuospatial | I | I | SI | I | |
AD, Alzheimer’s disease; HD, Huntingdon disease; I, impaired; N, normal; PD, Parkinson disease; PSP, progressive supranuclear palsy; SI, severely impaired. | |||||
XI. Evaluation
Good history and physical, with family and good mental status examination
CT without contrast initially
EEG may be required in some cases
Electrocardiogram
Urinalysis
Serum for the following: CBC, chem 18 (with electrolytes and LFTs), thyroid function tests, B12, rapid plasma reagin, erythrocyte sedimentation rate, antinuclear antibody, rheumatoid factor
Note: Consider the following in younger patients or if initial workup is negative: cortisol, Wilson workup, porphyria workup, 24-hour urine for heavy metals, HIV, purified protein derivative, angiotensin-converting enzyme level, vitamin E, very long chain fatty acid
Lumbar puncture if indicated (with cytology, AFB and fungal stains, angiotensin-converting enzyme level, multiple sclerosis profile, and so forth)
Neuropsychologic testing if trouble with diagnosis
Arteriogram/brain biopsy as indicated
XII. General Management (Specifics depend on underlying cause)
Rule out treatable causes early.
Incurable dementias
Pharmocologic treatment of neuropsychiatric symptoms (see table below)
Psychosis
Drug
Trade Name
Starting dose
Max dose
Atypical Antipsychotics
Risperidone
Risperdal
0.5 mg/d
1-3 mg/d
Olanzapine
Zyprexa
2.5 mg/d
5-10 mg/d
Quetiapine
Seroquel
12.5-25 mg/d
50-150 mg/d
Clozapine
Clozaril
6.25-12.5 mg/d
25-100 mg/d
Typical Neuroleptic (high potency)
Haloperidol
Haldol
0.25-0.5 mg/d
2-4 mg/d
(mid potency)
Loxapine
Loxitane
2.5-5 mg/d
10-20 mg/d
(low potency)
Thioridazine
Mellaril
10-30 mg/d
100-300 mg/d
Agitation / Aggression
Class
Drug
Trade Name
Starting Dose
Max Dose
Antipsychotics (same as listed above)
Anticonvulsants
Divalproex
Depakote
125 bid
1,500-2,000mg/d
Carbamazepine
Tegretol
50-100 mg/d
500-800 mg/d
Antidepressants
Trazadone
Deseryl
25-50 mg/d
200-300 mg/d
Paroxetine
Paxil
5-10 mg/d
40 mg/d
Sertraline
Zoloft
25-50 mg/d
150-200 mg/d
Citalopram
Celexa
10-20 mg/d
40 mg/d
Escitalopram
Lexapro
Venlafaxine
Effexor
75 mg/d
375 mg/d
Anxiolytics
Buspirone
BuSpar
5 mg bid
45 mg/d
Lorazepam
Ativan
0.5 mg/d
4-6 mg/d
Others
Propranolol
Inderal
10 mg bid
50-240 mg/d
Depression
Drug
Trade Name
Starting Dose
Max Dose
Selective Serotonin Reuptake Inhibitors
Fluoxetine
Prozac
10 mg/d
20-40 mg/d
Paroxetine
Paxil
5-10mg/d
40 mg/d
Sertraline
Zoloft
25-50 mg/d
150-200 mg/d
Citalopram
Celexa
10-20 mg/d
40 mg/d
Fluvoxamine
Luvox
50 mg/d
300 mg/d
Tricyclics
Nortriptyline
Pamelor
10 mg/d
50-100 mg/d
Desipramine
50 mg/d
150 mg/d
Others
Nefazodone
Serzone
150 mg bid
600 mg/d
Venlafaxine
Effexor
75 mg/d
375 mg/d
Anxiety
Drug
Trade Name
Starting Dose
Max Dose
Buspirone
BuSpar
5 mg/d
30-45 mg/d
Lorazepam
Ativan
0.5 mg/d
2-6 mg/d
Oxazepam
Serax
10 mg/d
30 mg/d
Sleep Disturbance
Drug
Trade Name
Starting Dose
Max Dose
Trazadone
Deseryl
50 mg/d
300 mg/d
Zolpidem
Ambien
5-10 mg/d
10 mg/d
Temazepam
Restoril
15 mg/d
30 mg/d
Zaleplon
Sonata
5-10 mg/d
10 mg/d
Nonphamacologic treatment of neuropsychiatric symptoms
Increased daytime activities
Music therapy
Environmental enhancement
Daycare
Specific caregiver-focused interventions
Interaction with knowledgeable professional and nonprofessional caregivers
Cognitive symptoms (see Alzheimer disease treatment)
Central Nervous System Degenerative Diseases
I. Dementias
Alzheimer disease
Epidemiology
The most common degenerative disease of the brain
10% of people over age 65 years have Alzheimer disease, and approximately two thirds of new cases of dementia over age 65 are attributable to Alzheimer disease.
Male = female, onset usually after age 60 years but can begin earlier
Risk factors: advanced age, family history, Down syndrome (all patients over age 35 years have Alzheimer disease), low educational level, chromosomal mutations on chromosomes 1, 14, and 21, apolipoprotein E ε – 4 genotype, history of brain injury, history of depression, female gender
Pathophysiology
Cleavage of the amyloid precursor protein by beta and gamma secretases produces the potentially cytotoxic Aβ fragment (primarily Aβ 40 and Aβ 42).
Extracellular aggregates of Aβ deposit in an insoluble β-pleated sheet configuration which may damage neuronal structure, inhibit synaptic transmission, and incite a cytotoxic inflammatory cascade: this produces many of the pathologic changes seen in the brains of Alzheimer disease patients.
Most familial cases are associated with one of four genetic defects: amyloid precursor protein, apoE ε 4 (most common mutation, lower age of onset), and presenilin 1 and 2 (associated with aggressive early onset).
Decreased choline-acetyltransferase in the hippocampus and neocortex caused by loss of cholinergic projections from the nucleus basalis of Meynert
Clinical features
Gradual decline of intellectual function
Poor short-term memory
Visuospatial disorientation
Language/speech problems—aphasia, anomia, and later echolalia, mutism
Apraxias—dressing, ideomotor
Personality changes and paranoid delusions not uncommon
Eventually bed bound, immobile, and mute
Motor and sensory functions spared until very late in disease
Seizures occur in approximately 10% of patients.
Imaging
CT/MRI (magnetic resonance imaging): atrophy of temporal, frontal, and parietal lobes (with relative sparing of the primary motor and sensory cortices), symmetric widening of the sylvian fissures and dilatation of the temporal horns
Positron emission tomography (PET): decreased metabolism in the bilateral parietal and temporal lobes
Single photon emission computed tomography: decreased blood flow in the bilateral parietal and temporal lobes
Pathologic findings
Senile plaques—argyrophilic with central amyloid core. Correlate best with severity of dementia. Contain extracellular deposits of amyloid β proteins.
Neurofibrillary tangles—intraneuronal cytoplasmic bundles of paired helical filaments; subunit of paired helical filaments is the microtubule-associated protein, tau (tau in tangles is hyperphosphorylated, insoluble, and paired with ubiquitin)
Granulovacuolar degeneration—seen in pyramidal cells of hippocampus
Amyloid—stains with congo red and has apple-green birefringence under polarized light. Found in plaque cores and in blood vessels (amyloid congophilic angiopathy)
Hirano bodies—eosinophilic, cytoplasmic inclusions in hippocampal cells
Decreased synaptic density, widespread loss of neurons in the cortex, nucleus basalis of Meynert (substantia innominata) and locus ceruleus
Tau-staining positive—increased in cells destined to undergo fibrillary degeneration
Formation of plaques and tangles represents one of several cytologic responses by neurons to the gradual accumulation of Aβ and Aβ associated proteins.
Other disorders with neurofibrillary tangles
Down syndrome (increased plaques and tangles)
Parkinson disease (helps to explain why approximately 30% of patients with Parkinson disease also develop dementia)
Dementia pugilistica—occurs in boxers, increased neurofibrillary tangles but not plaques
Postencephalitic parkinsonism
Progressive supranuclear palsy
Parkinson disease/dementia/ALS complex of Guam
Subacute Sclerosing Panencephalitis
Kuf disease
Diagnosis
DSM IV criteria are reliable to diagnose dementia of the Alzheimer disease type.
No imaging (functional or structural), genetic, or biochemical laboratory test can be routinely recommended for diagnosing Alzheimer disease (2001 AAN Practice Parameter).
Treatment (Currently available treatments are based on cholinergic hypothesis, which states that there is a selective loss of cholinergic cell bodies and enzymes necessary for normal congnition.)
Rule out reversible causes of dementia.
Tacrine (tetrahydroaminoacridine)—a reversible acetylcholinesterase inhibitor. Rarely used.
Donepezil (Aricept)
Not associated with significant hepatotoxicity
Mild cholinergic side effects (such as nausea, vomiting, diarrhea)
Begin at 5 mg every day and increase to 10 mg every day after 4 weeks.
Rivastigmine (Exelon)
Not associated with significant hepatotoxicity
Inhibits acetylcholinesterase and butyrylcholinesterase
Substantial cholinergic side effects with rapid titration (should be given with food)
Begin at 1.5 mg two times a day and titrate to 3 to 6 mg two times a day
Galantamine (Reminyl)
Not associated with significant hepatotoxicity
Acetylcholinesterase inhibitor and nicotinic receptor modulator
Begin at 4 mg two times a day and increase to 8 to 12 mg two times a day, with 4 weeks between dose increases (lessens the likelihood of cholinergic side effects)
All the cholinesterase inhibitors have a broad range of efficacy, which includes cognition, behavior, and function. These drugs provide temporary stabilization of Alzheimer disease-related deterioration.
Memantine (Namenda)
N-Methyl-D-aspartate receptor antagonist
Starting dose, 5 mg daily
Maximum dose, 10 mg two times a day
Memantine may have a synergistic effect in combination with cholinesterase inhibitors and is typically used in combination with one of these medications.
Vitamin E – 1,000 IU two times a day significantly delayed functional decline, institutionalization, and death in moderate Alzheimer disease in one study.
Selegeline
Same results as with vitamin E
5 mg two times a day dose
Symptomatic treatment of behavioral problems and agitation
Supportive care for the patient and caregivers
Prevention
Postmenopausal estrogen replacement may be effective, although studies are not in agreement.
Anti-inflammatory drugs—observational studies show an approximate 50% reduction in Alzheimer disease risk for users of nonsteroidal anti-inflammatory drugs for 2 or more years
Potentially preventive—red wine, HMG-CoA reductase inhibitors, antioxidants
Pick disease (a frontotemporal demetia)
Epidemiology
Rare
Onset usually in sixth decade of life
Females > males
Clinical features
Personality changes and behavioral problems—apathy, abulia, frontal release signs (frontal lobe involvement). Poor judgment is a hallmark.
Aphasia (temporal lobe involvement)
Klüver-Bucy-type syndrome may occur (hypersexual, hyperoral, docile)
Generalized cognitive decline (usually sparing praxis and visuospatial function)
Disturbed behavior is usually the presenting symptom.
Imaging—CT/MRI: Characteristic atrophy of the frontal and temporal lobes (“Pick’s at poles”) with relative sparing of the posterior third of the superior temporal gyrus and primary motor and sensory cortices
Pathologic findings
Neuronal loss in layers I through III
Pick bodies—argyrophilic, intracytoplasmic inclusions
Ballooned neurons (also seen in cortical-basal ganglionic degeneration)
Other frontotemporal dementias
All clinically similar to Pick disease, but lack its distinctive pathologic findings
Are progressive
Involve loss of judgment, accompanied by disinhibition, social misconduct, apathy and/or aphasia
Behavioral changes are worse than memory loss
Variants include primary progressive aphasia, dementia plus upper or lower motor neuron dysfunction, progressive subcortical gliosis, familial form localizing to chromosome 17.
Account for 5% to 10% of dementias in most neurology practices
Onset in the sixth decade
Dementia with Lewy bodies
Epidemiology
Thought to be second leading cause of dementia; underrecognized
Age at onset typically 50 to 80 years (average age, 72)
Male > female (2:1)
Clinical features
Triad: (1) dementia, (2) psychosis, (3) mild extrapyramidal symptoms
Presenting symptoms: commonly neurobehavioral; disinhibition and psychiatric problems in 30% to 50%, frank psychosis in approximately 30%; mild delusions and visual hallucinations as well as executive dysfunction are early features
Extrapyramidal symptoms: mostly rigidity and bradykinesia; tremor is rare and occurs late if at all. Dementia is far worse than the movement disorder. May have transient lapses of consciousness
Pathologic findings
Lewy bodies—eosinophilic, cytoplasmic inclusions found throughout the cortex and in pigmented neurons of the brainstem
Stain with ubiquitin (especially in CA 2 and 3 regions of hippocampus)
Tau-negative, amyloid-negative, Alzheimer-type pathologic changes are seen in 50% to 75% of cases (mainly plaques)
Vascular dementia—can be caused by ischemic stroke of any type, cerebral hemorrhage, anoxic/ischemic injury, or vasculitis
Epidemiology
Usually in those with history of stroke, risk factors for vascular disease
Frequency is approximately 10% of all dementias
Male > female
Clinical features
Clinical features can be scored using the Hachinski scale:
A score of >7 suggests multi-infarct dementia.
A score of ≤4 indicates probable primary degenerative dementia.
Clinical Finding
Score
Abrupt onset
2
Fluctuating course
2
History of stroke
2
Focal neurologic symptoms
2
Focal neurologic signs
2
Stepwise deterioration
1
Nocturnal confusion
1
Preservation of personality
1
Depression
1
Somatic complaints
1
Emotional incontinence
1
Hypertension
1
Evidence of atherosclerosis
1
May be associated with pseudobulbar palsy (dysphagia, dysarthria, emotional and urinary incontinence, increased jaw jerk and facial reflexes) resulting from multiple bilateral lacunar infarctions. Gait disturbance may also be present.
Prominent frontal / executive function with less language impairment than in Alzheimer disease
Imaging and pathologic findings
Usually evidence of bilateral cerebral infarctions
MRI evidence of disease of >25% of cerebral white matter
Treatment—aimed at stroke prevention (control of hypertension, and so forth)
Normal pressure hydrocephalus
Epidemiology: age typically >60 years for the idiopathic form
Clinical features (classic triad)
Dementia
Gait disturbance: short steps and broad-based, typically precedes dementia and urinary incontinence
Urinary incontinence: poor realization of the need to void
Pathologic findings
Cerebrospinal fluid (CSF) pressure typically <18 cm of water, but transient higher pressures may occur
Imaging
Ventricular enlargement with possible transependymal flow
Ventricular cisternography: delayed radionucleotide washout study
Treatment
Shunt placement
Outcome best when shunt placed prior to dementia or urinary incontinence
Other diseases associated with dementia
Prion diseases (such as Creutzfeldt-Jakob, Gerstmann-Straussler-Scheinker)
Thalamic dementia (rare syndrome of pure degeneration of the thalamus, subacute dementia, choreoathetosis)
Mitochondrial disorders (myoclonic epilepsy with ragged red fibers [MERRF], mitochondrial encephalomyopathy, lactic acidosis, and strokelike syndrome [MELAS])Related posts:
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