Download presentation
Presentation is loading. Please wait.
1
Vascular dementia (Multi-infarct dementia)
The second most common (15-25%) form of dementia. Caused by microvascular disease in the brain that produces multiple small infarcts. A substantial infarct burden must accumulate before dementia develops.
2
Risk factors Stroke DM HT APOe4 M:W is 2:1
3
Clinical manifestations
Step-wise loss of function as the microinfarcts add up no specific pattern of cognitive deficits. Neuropsychological testing may not differentiate vascular Dementia from AD. Lateralizing signs: Spasticity, hemiparesis, ataxia, pseudobulbar palsy (inability to control facial movement) Depression, anger and paranoia are common.
4
Treatment No truly effective treatment
Physical and emotional support, proper nutrition, exercise, and supervision cholinesterase inhibitors (successful tt) AntiHTN may prevent onset of vascular demintia
5
VASCULAR DEMENTIA VERSUS ALZHEIMER’S
Since vascular dementia is caused by small brain infarcts, patients also have focal neurological symptoms (such as hyperreflexia or paresthesias). Onset is usually more abrupt than Alzheimer’s. Greater preservation of personality. Can reduce risk by modifying risk factors (such as smoking, hypertension, and diabetes).
6
Lewy body dementia LBD The third most common dementia (10-15%)
Caused by lewy bodies and lewy neurites in the brain (primarily in the basal ganglia). LEWY BODIES
7
Clinical manifestations
Progressive cognitive decline. Waxing and waning of cognition. Parkinsonism. Visual hallucinations. Sensitivity to neuroleptics (antipsychotics). Paranoid delusions REM sleep behavior disorders is common. Core features
8
Diagnosis Strong similarity to Parkinson disease dementia: In LBD:
In PD: Onset of Parkinsonism 12 months Dementia Dementia
9
Treatment Cholinesterase inhibitors may help improve visual hallucinations. Psycho-stimulants, L-Dopa and Carbi-Dopa, and dopamine agonists may improve cognition, apathy and psychomotor slowing. Atypical Neuroleptics have been slightly effective in stopping delusions. Clonazepam treatment for REM sleep behavioral disorders.
10
Huntington’s Disease Autosomal dominant genetic disorder that results in progressively disabling cognitive, physical, and psychological functioning, ultimately resulting in death after approximately 15 years Involves loss of GABA-ergic neurons in basal ganglia CLINICAL MANIFESTATIONS Onset: 35 to 50 years of age Hallmarks: Progressive dementia choreiform movements (dancelike flailing of arms and legs) Muscular hypertonicity Depression and psychosis very common
11
PATHOLOGY Trinucleotide repeat (CAG) on short arm of chromosome 4; primarily affects basal Ganglia. Involves loss of GABA-ergic neurons in basal ganglia DIAGNOSIS MRI shows caudate atrophy (and sometimes cortical atrophy). Genetic testing and MRI are diagnostic. TREATMENT There is no effective treatment available (supportive only).
14
Parkinson’s Disease * Progressive disease with prominent neuronal loss in substantia nigra, which provides dopamine to the basal ganglia, causing physical and cognitive impairment. Approximately 30% of patients with Parkinson’s disease develop dementia. 50% will suffer from depression. Slightly more in men
16
CLINICAL MANIFESTATIONS
Bradykinesia (slowness in the execution of movement) Cogwheel rigidity Resting tremor Mask facial expression Shuffling gait Dysarthria (abnormal speech)
18
ETIOLOGY Idiopathic (most common) Traumatic Drug- or toxin-induced Encephalitic Familial (rare) PATHOLOGY AND PATHOPHYSIOLOGY Loss of cells in the substantia nigra of the basal ganglia, which leads to a decrease in dopamine and loss of the dopaminergic tracts
19
TREATMENT Levodopa—degraded to dopamine by dopadecarboxylase
Pharmacologic Levodopa—degraded to dopamine by dopadecarboxylase Carbidopa—peripheral dopadecarboxylase inhibitor prevents levodopa from being converted to dopamine before it reaches the brain. Amantadine—mechanism unknown Anticholinergics—help relieve tremor Dopamine agonists (bromocriptine, etc.) Monoamine oxidase (MAO)-B inhibitors (selegiline)—inhibit breakdown of dopamine Levodopa crosses the blood–brain barrier (BBB). Carbidopa does not. Carbidopa prevents conversion of levodopa to dopamine in the periphery. Once levodopa crosses BBB, it is free to be converted to dopamine. Antipsychotic medications exacerbate demintia in parkinson dis
21
Creutzfeldt-Jakob disease CJD
A rapidly progressive degenerative disease of the CNS caused by accumulation of abnormal forms of prions. Affects older patients, and may be inherited, sporadic or acquired. A small percentage of pt. have become infected through corneal transplant
22
Clinical manifestations
Rapidly progressive dementia 6-12 months after onset of symptoms. More than 90% of patients have myoclonus (sudden spasm of muscles). Basal ganglia and cerebellar dysfunctions are common. Personality changes, immature behavior and paranoia are early signs. Rapid progression to stupor, coma and death in a matter of months to a few years.
23
Diagnosis Definitive: Pathological demonstration of spongiform changes of brain tissue.
24
Probable: The presence of rapidly progressive dementia and Periodic Generalized Sharp Waves on EEG + two or more of the following Myoclonus. Cortical blindness. Ataxia, pyramidal signs or extrapyramidal signs. Muscle atrophy. Mutism.
25
Incurable and Invariably fatal!
Treatment Incurable and Invariably fatal!
26
Pick’s Disease/ Frontotemporal Dementia (FTD)
Typically between years. 20-30% are familial. Mean duration of illness to death: 4-6 years CLINICAL MANIFESTATIONS: Profound changes in personality and social conduct. Disinhibited verbal, physical and sexual behavior. Echolalia, overeating, oral exploration of inanimate objects. Lack of emotional warmth, empathy and sympathy. Poor insight about behavioral alterations. Cognitive deficits in attention, abstracting, planning and problem solving. Memory, language and spatial functions are well preserved. Kluver bucy syndrome * hyerphagia , hypersexuality
27
PATHOLOGY Atrophy of frontotemporal lobes. Pick bodies— intraneuronal inclusion bodies (not necessary for diagnosis of FTD) TREATMENT: * Anticholinergic medications and antidepressants have consistently shown to improve behavioral symptoms but not cognition.
29
HIV associated dementia
HAD is the most common dementia caused by infectious disease. The prevalence increases as the patient lives longer. Caused by: The direct effect of the virus on the cells. Infections due to neutropenia
30
Risk factors: Duration of the illness. Low CD4. High viral loads Clinical manifestations: Rapid decline in cognition, behavior and motor ability. Poor memory and impaired concentration. Psychomotor retardation. Apathy and social withdrawal. Depression. Preserved language. Treatment: HAART Psychostimulants.
31
Normal Pressure hydrocephalus
NPH is a reversible cause of dementia. Patients have enlarged ventricles with no increased CSF pressure. Etiology idiopathic secondary to obstruction of CSF reabsorption sites due to( trauma, infection, or hemorrhage). * Clinical triad: 1. Gait disturbance (often appears first) Wobbly 2. Urinary incontinence Wet 3. Dementia (mild, insidious onset) Wacky TREATMENT Relieve increased pressure with shunt. Of the clinical triad, the dementia is least likely to improve.
32
Thank You
Similar presentations
© 2025 SlidePlayer.com Inc.
All rights reserved.