1. Dementia Definition : It is defined as an acquired deterioration in cognitive abilities that impairs the successful performance of activities of daily living.

2. Anatomy Of The Dementia : Dementia results from the disruption of cerebral neuronal circuits; the quantity of neuronal loss and the location of affected regions are factors that combine to cause the specific disorder. Behavior and mood are modulated by noradrenergic, serotonergic, and dopaminergic pathways, while acetylcholine seems to be particularly important for memory.Therefore, the loss of cholinergic neurons in Alzheimer’s disease (AD) may underlie the memory impairment, while in patients with non-AD dementias, the loss of serotonergic and glutaminergic neurons causes primarily behavioral symptoms, leaving memory relatively spared.

3. Causes & Evaluation of patient with dementia :

4. ALZHEIMER’S DISEASE The cognitive changes with AD tend to follow a characteristic pattern, beginning with memory impairment and spreading to language and visuospatial deficits. In the early stages of the disease, the memory loss may go unrecognized or be ascribed to benign forgetfulness. Once the memory loss begins to affect day-to-day activities, the disease is defined as MCI(minimal cognitive impairmaent). Approximately 50% of MCI individuals will progress to AD within 5 years.. The presence of amyloid plaques and neurofibrillary tangles characteristic of Alzheimer disease.

5. Language becomes impaired—first naming, then comprehension, and finally fluency. In some patients, aphasia is an early and prominent feature. Word finding difficulties may be a problem even when formal testing demonstrates intact naming and fluency. Apraxia emerges, and patients have trouble performing sequential motor tasks. Visuospatial deficits begin to interfere with dressing, eating, solving simple puzzles, and copying geometric figures. Patients may be unable to do simple calculations or tell time, In the late stages of the disease, some persons remain ambulatory but wander aimlessly. Loss of judgment, reason, and cognitive abilities is inevitable. Delusions are common and usually simple in quality, such as delusions of theft, infidelity, or misidentification.

6. They may show hyperactive tendon reflexes. Myoclonic jerks (sudden brief contractions of various muscles or the whole body) may occur spontaneously or in response to physical or auditory stimulation, Often death results from malnutrition, secondary infections, pulmonary emboli, or heart disease. The typical duration of AD is 8–10 years, but the course can range from 1 to 25 years. For unknown reasons, some AD patients show a steady downhill decline in function, while others have prolonged plateaus without major deterioration.MRI either normal or show hipoccampal atrophy

7. TREATMENT OF AD Donepezil, rivastigmine, galantamine, memantine, The pharmacologic action of donepezil, rivastigmine, and galantamine is inhibition of cholinesterase, with a resulting increase in cerebral levels of acetylcholine. Memantine appears to act by blocking overexcited N-methyl-D-aspartate (NMDA) channels. some drugs have good effect on cognitive function in patient with AD but need more confirmation like ginko biloba, vit. E,estrogen replacement therapy. Treatment of depression by SSRI, treatment of seizure by phenytoin, carbamazepine. psychosis treated by atypical antipsychotics like resperidon.care of pulmonary function,good nursing with good nutrition by caregiver.

8. Frontotemporal Dementia The fronto-temporal dementias, including Pick disease, sometimes can be distinguished from Alzheimer disease during life by: their generally earlier onset, more prominent behavioral (personality) than cognitive (memory) dysfunction at presentation, preferential atrophy of the frontal and anterior temporal lobes on CT scan or MRI of the brain. Definitive diagnosis is usually not possible during life, and relies instead on histo-pathological features which include the presence of Pick cells and Pick inclusion bodies. Familial occurrence of fronto-temporal dementia has been documented.There is no specific treatment, just symptomatic, SSRI may be beneficial.

9. LEWY BODY DEMENTIA Pathology of lewy body similar to that found in the substantia nigra in Parkinson's disease is found in LB in the cerebral cortex (i.e: Lewy bodies). This condition usually presents as cognitive impairment in the context of an extrapyramidal syndrome, and the cognitive features may be indistinguishable from those of Alzheimer's disease. Patients' cognitive state often fluctuate with visual hallucinations. they have a high sensitivity to the neuroleptic drugs. Treatment by rivastigmen, mimantin, or donpezil.

10. VASCULAR DEMENTIA Either: 1.Multi-infarct dementia which is of 2 type: multiple large cortical infarcts from occlusion of major cerebral arteries or several smaller infarcts (multi-lacunar state) affecting sub-cortical white matter, basal ganglia, or thalamus. 2. Diffuse white matter disease Patients with multi-infarct dementia have a history of hypertension, a stepwise progression of deficits, a more or less abrupt onset of dementia, andfocal neurologic deficits. Examination commonly shows pseudo-bulbar palsy, focal motor and sensory deficits, ataxia, gait apraxia, hyper-reflexia, and extensor plantar responses.

11. Investigative Studies: The MRI in multi-infarct dementia may show multiple large cortical or small subcortical lacuncies. MRI is more sensitive than CT for detecting these abnormalities. VASCULAR DEMENTIA due to chronic hypertention

12. Treatment : Hypertension, when present, should be treated to reduce the incidence of subsequent infarction and to prevent other end- organ diseases. Optimum control of blood sugar if patient is diabetic. Antiplatelet & lipids lowering agents may help to reduce the risk of future strokes. Anticholinesterases such as Donepezil (5 mg/day for 1 month then increase to 10 mg) also affective mode of treatment here as for Alzheimer’s disease.

13. Normal Pressure Hydrocephalus consisting of an abnormal gait (ataxic or apractic), dementia (usually mild to moderate), and urinary incontinence. Neuroimaging findings in NPH are those of a communicating (non-obstructive) hydrocephalus with a patent aqueduct of Sylvius. In many cases periventricular edema is present. There is no evidence of cortical or hippocampal atrophy. Lumbar puncture findings include an opening pressure in the high-normal range and normal CSF sugar, cells, protein. It is caused by obstruction to normal flow of CSF over the cerebral convexity (i.e.: obstruction outside the ventricular system) and delayed absorption into the venous system. Some cases due to over-production of C.S.F by choroid plexus.

14. The indolent nature of the process results in enlarged lateral ventricles but relatively little increase in CSF pressure. The exact cause of the clinical syndrome is unclear. Some cases are idiopathic while other being secondary to conditions producing scarring of the basilar meninges (blocking upward flow of CSF) such as previous meningitis, subarachnoid hemorrhage, or head trauma. Treatment by ventriculoatrial, ventriculoperitoneal, or lumboperitoneal shunting surgery.

15. CT Brain in pt. with NPH

16. Wernick –Korsakoff Disease Deficiency of thiamin (vitamin B1) usually presents with an acute confusional state (Wernicke's encephalopathy) and brain-stem abnormalities such as ataxia, nystagmus and extraocular muscle weakness, particularly lateral rectus weakness. If inadequately treated, this results in a dementia characterized by a profound disturbance of short-term memory associated with a tendency to confabulate (i.e: tendency to full the gabs in memory by imaginary events created by the patient), called Korsakoff's syndrome. The deficiency can arise as a result of malnutrition (particularly when due to chronic alcohol misuse), malabsorption or even protracted vomiting (as in hyperemesis gravidarum). The diagnosis is usually made clinically.

17. Because it is potentially treatable at the stage of Wernicke’s encephalopathy, the condition must be considered in any confused or demented patient; if there is any doubt, it is usually better to treat anyway. Treatment consists of intravenous thiamin 100 mg before or with dextrose to avoid exacerbating the disease. Parenteral thiamin should continue till patient regain the ability for normal dieting. In addition we should treating the underlying cause. Once Korsakoff’s syndrome develop the condition became irreversible.

18. Vit. B12 Defeciency This disease occurs due to low B12 level either due to vegetarian state or due to malabsorption like perinicious anemia or celiac, pt. presented with peripheral neuropathy, impaired postion and vibration sensation, abscent ankle jerk, sensory ataxia with steppage gait,optic atrohhy,pyramidal signs in the form of spastic paraplegia, bilat. Extensor planter and brisk knee jerk, if pt. not treated at this stage may pass to dementia and psychosis. Diagnosed by measuring s. B12 level or more specific by measuring s. methylmelonic acid. Treated by IM B12. Injection and correct the underlying cause.