neurocognitive disorders

Neurocognitive Disorders

Nazar M Mohammad Amin

Professor of PsychiatryM B Ch B, D P M, M R C Psych., F R C Psych., F A C P

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Neurocognitive disorders in DSM 5 include

Delirium and followed by syndromes of Major Neurocognitive Disorder (NCD) and Mild Neurocognitive disorder.

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Both types of NCD have subtypes

NCD due to Alzheimer’s disease,Vasculsar NCDNCD with Lewy bodiesNCD due to parkinson’s diseaseFrontotemporal NCDNCD due to traumatic brain injuryNCD due to HIV infectionSubstance/medication induced NCD

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NCD due to Huntington’s DiseaseNCD due toPrion’s diseaseNCD due to another medical conditionNCD due to multiple etiologiesUnspecified NCD

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• Cognitive deficits are present in many mental disorders but only disorders whose core features are cognitive are included in the NCD category.

• The cognitive decline was not present from birth or very early in life therefore represent a decline from a previously attained level of functioning.

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Neurocognitive DisordersDelirium

• Is a disturbance in attention and awareness of the environment, develops over a short period of time( hours to a few days), tends to fluctuate in severity during the course of a day, with additional cognitive disturbance as memory,orientation,language, perception and others, is not due to another neurocognitive disorder or in the context of severely reduced level of arousal such as coma, and there is evidence that disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal or exposure to toxin or is due to multiple etiologies.

DSM 5 6


Clinical featuresThe cardinal feature is disturbed consciousness as drowsiness, decreased awareness of the surroundings, disorientation and distractibilityThere is mental slowness, perceptual abnormalities, and disorganization of sleep wake cycle.It is worse at night There is restlessness and hyperactivity or hypoactive with retardation and perseveration.

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Clinical features cont

Thinking is slow and muddled .Ideas of reference, persecutory delusions which are transient and poorly elaborated.Misinterpretation and illusions, visual hallucinations, tactile and auditory hallucinations.Anxiety, depression and emotional labilityDepersonalization and derealizationImpaired attention and registration leads to amnesia for the period of the delirium. 8


Causes of delirium:•Drugs & alcohol intoxication, withdrawal and delirium tremens, opiates, prescribed drugs, Antiochinergics, sedatives, digoxin, diuretics, lithium, and steroids.

•Medical conditions, febrile illnesses, septicemia, organ failure( cardiac, renal, hepatic), hyper or hypoglycemia, postoperative hypoxia, Thiamine deficiency

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Causes of delirium: cont

•Neurological conditions, epileptic seizures or post

ictal, head injury, space occupying lesions, encephalitis,cerebral hemorrhage

•Constipation, dehydration, pain and sensory deprivation.

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Management of delirium

It is a medical emergencyoThe underlying cause must be treated drugs must suspected as a common cause

Urgent investigations are necessary

General measures to relieve distress, control agitation and prevent exhaustion

Frequent explanation, reorientation, and reassurance.oAvoid unnecessary staff changes and encourage relatives to be with the patient, nursing in a quiet single room with adequate lighting 11


Management of delirium cont

Drug treatmentUsed to treat the underlying cause, control agitation and distress and allow adequate sleep.Haloperidol is used and some cases are treated with atypical antipsychotics. Atypical antipsychotics should be avoided in dementia especially with Lewy bodies, and in epilepsy and withdrawal from alcohol (DT).

Chlordiazepoxide is used in DTs.12


Outcome

Many cases recover rapidlyThe outcome is worse in the elderly, preexisting dementia or physical illness.Delirium in the elderly increases the risk of death in the next two years, institutionalization and risk of dementia.

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Neurocognitive Disordersamnesia and amnesic syndromes

Amnesia Is Loss Of Memory For Episodic Memory As Anterograde Amnesia And Retrograde Amnesia.

It Is Associated With Social And Occupational Dysfunction And Evidence Of A General Medical Condition.

Amnesia Occurs In The Absence Of Evidence For Generalized Intellectual Dysfunction.

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Causes of amnesia: TransientTransient global amnesiaTransient epileptic amnesiaHead injuryAlcoholic blackoutsPost ECT PTSDPsychogenic fugueAmnesia for criminal offence

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Causes of amnesia: persistent

Korsakov syndromeHerpes encephalitisPosterior cerebral artery and thalamic strokesHead injury

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Clinical featuresProfound deficit in episodic memoryDisorientation for timeLoss of autobiographical informationAnterograde amnesia for verbal and visual materialLack of insightNew learning is impaired but retrograde amnesia is partially preserved

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Korsakov syndrome also called

Wernicke Korsakov Syndrome

A syndrome that follows Wernicke’s encephalopathy

Delirium, ataxia, pupillary abnormalities, ophthalmoplegia, nystagmus, and peripheral neuropathy

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It is due to thiamine deficiency caused by alcohol abuse, hyperemesis gravidarum, severe malnutrition, or due to infarction, tumors or infection

There is neuronal loss, gliosis and microhemorrhages in the periaqueductal and periventricular gray matter

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It is regarded as a medical emergency

And diagnosed by decreased red cell transketolase level and increased MRI signal in midline structures

Treatment is by replacing the thiamine before administering glucose

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Transient global Amnesia

Occurs in middle or late lifeThere is sudden onset of isolated ,often profound, anterograde amnesia in a clear consciousness ,

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Dementia

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Is an acquired global impairment of intellect, memory, and personality without impairment of consciousness.

The main complaint is poor memory .

Disturbance of behavior, language, personality, mood or perception.

Dementia

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It is often precipitated by intercurrent illness or change in social circumstances.

Amnesia, impaired attention and concentration with difficulty in new learning, the amnesia is for recent events to start with and then involve more remote material.

Dementia

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Loss of flexibility and adaptability and if you press the patient who lost this flexibility, there will be sudden explosions of anger or grief(catastrophic reaction).

Self neglect and avoids social engagements.

Disorientation for time and then for place and person.

Dementia

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Aimless behavior

Slow thinking with perseveration

False ideas, mostly persecutory

Speech becomes incoherent or mute.

Dementia

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Behavioral, affective, and psychotic features accompany the cognitive deficits.

Insight is retained at first but gradually lost. Depression, anxiety, distress, irritability

and aggression occurs. Later affect becomes blunted. Hallucinations and delusions could appear

too.

Dementia

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there are special tools to screen for cognitive impairment such as MMSE (Mini-Mental State Examination).

Diagnosis and finding the cause requires the following investigations:

Full blood count and ESR, urea and electrolytes, liver function tests, calcium and phosphate, thyroid function tests, Vitamin B12 and Folate, MRI and CT brain scan, urinalysis, syphilis serology, HIV status, CXR, Neuropsychological assessment, Genetic testing and EEG.

Dementia

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Risk assessment include:

Self neglect, poor judgment, wandering, abuse, disinhibition, aggression, exploitation by relatives, fitness to drive and aggression toward others.

Dementia

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Alzheimer’s disease

60% of dementia is due to Alzheimer disease2-7% of the population aged over 65years.The prevalence increases with increasing age.

DementiaAlzheimer’s disease

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clinical featuresAmnesia, gradual and progressive

Aphasia

Apraxia

Agnosia

Disturbance in executive functioning e.g. planning and reasoning

Depression

Psychosis (delusions and hallucinations)

behavioural symptoms e.g. agitation and wandering

Personality change (reduction in drive, aggression, sexual disinhibition)

Median survival from diagnosis is 5-7 years.


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Neuropathology The brain is shrunken, widened sulci, enlarged ventricles, brain

weight is reduced. Neurofibrillary tangles, and senile plaques(amyloid plaques) There is selective loss of neurons in the hippocampus and

entorhinal cortex, gliosis, and loss of synapses. The protein at the heart of the senile plaques is β amyloid.


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Aetiology

Genes.

Most of the cases are not genetically inherited but in rare cases it is familial and causative mutations were identified in three genes, APP(amyloid precursor protein, presenilin1 and presenilin 2.

Environmental factors include past history of depression, diabetes mellitus, obesity, aluminum exposure and head injury.


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NSAIDs, hormone replacement, and statins are protective.

Other theories include cholinergic hypothesis based on the loss of acetylcholine in the cerebral cortex.

The role of oxidative stress, inflammation, and apoptosis(programmed cell death).

Dementiavascular dementia

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Is the second commonest cause of dementia.

More in men than women, more in Japan, China and Russia.

Clinical features:

It appears in the late sixties or seventies.

Emotional and personality changes appear first followed by impairment of memory and intellect.


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Depression, emotional liability and confusion

Behavioral retardation and anxiety

Transient Ischemic attacks or mild strokes are common.

The course is stepwise with periods of deterioration and partial recovery.

They have shorter survival than Alzheimer patients.


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They have signs of hypertension, arteriosclerosis in the peripheral and retinal vessels and signs of focal neurological deficits.

The etiological factors include the same for cerebrovascular diseases including diabetes, hypertension, hyperhomocysteinaemia.

It is possible to have both Alzheimer's dementia and vascular dementia in the same patient at the same time.

DementiaDementia with Lewy Bodies

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Is the second or third most frequent cause of dementia

The cardinal feature is Lewy bodies in the cerebral cortex.

Main clinical features include fluctuating level of dementia, recurrent delirium like phases, parkinsonism and visual hallucinations

DementiaDementia with Lewy Bodies

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Neuropathology Presence of Lewy bodies in the cerebral cortexThey are seen in the substantial nigraPresence of α-synuclein and ubiquitin proteins.

DementiaFrontotemporal Dementias

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Is the second most common form of presenile dementia.

Presentation is usually between 45&70 years of age.

Prominence of behavioral rather than cognitive features.


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The frontal form present with behavioral and personality change and the temporal form with language disorder.

There are familial and sporadic cases.10%of the cases are autosomal dominant.


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Subtypes include :

Pick’s disease.Semantic dementia


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On neuroimaging there is focal and asymmetrical atrophy of the temporal and frontal poles.

EEG is usually normal unlike the diffuse slowing in Alzheimer's disease.

Acetylcholine and dopamine are not affected but serotonin markers are reduced.

Thank you43

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