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Here is a compilation of essays on ‘Organic Mental Disorders’ for class 11 and 12. Find paragraphs, long and short essays on ‘Organic Mental Disorders’ especially written for school and college students.
Essay on Organic Mental Disorders
Essay Contents:
- Essay on Delirium
- Essay on Dementia
- Essay on Organic Amnestic Syndrome
- Essay on Organic Delusional Disorder
- Essay on Organic Hallucinosis
- Essay on Organic Mood Syndrome
- Essay on Organic Personality Syndrome
- Essay on Organic Anxiety Syndrome
- Essay on Organic Catatonic Disorder
1. Essay on Delirium:
Among the organic mental syndromes, delirium is the most common. The essential characteristic of delirium is a clouded state of consciousness i.e., a reduction in state of consciousness i.e., a reduction in the clarity of awareness of the environment.
This is manifested by difficulty in sustaining attention to the external stimuli, sensory misperception, disturbances in level of arousal and psychomotor activity and a disordered stream of thought.
Epidemiology:
Delirium is the mental disorder with the highest incidence. About 10 to 25 per cent of medical-surgical inpatients and about 20 to 40 percent of geriatric patients meet criteria for delirium during hospitalization. The prevalence in the community is low. It can occur at any age.
Etiology:
The common causes of delirium are same as given in Table 13.2 (Mnemonic “Vindictive Mad”).
Clinical Picture (Table 13.4):
i. Disturbed psychomotor activity presenting as restlessness, hyperactivity, aimless groping or picking at the bed clothes (fioccillation), a coarse tremor and unsteadiness of the hands asterixis (irregular flapping movements of the hyperextended hands, dorsiflexed wrists in hepatic, renal and respiratory failure), Myoclonic jerking.
ii. Autonomic signs such as tachycardia, sweating, flushed face.
Course:
Delirium usually develops over a short period of time. It begins quite abruptly.
The duration of an episode is usually brief, about one week.
The complications of delirium may be due to injuries (falling out of bed due to frightening hallucination), agitation (may interfere with medical treatment; or may cause injuries to neighbouring patients, hospital personnel or suicide, dementia, and rarely Amnestic syndrome or Organic personality syndrome.
Differential Diagnosis:
(a) Dementia:
The clinical comparison between delirium and dementia is given in Table 13.1:
(b) Other Organic Disorders:
Other organic disorders e.g., organic hallucinosis or organic delusional disorder.
(c) Functional Psychoses:
Functional psychoses e.g., Schizophrenia and other psychotic disorders.
(d) Factitious Disorder with Psychological Symptoms:
Inconsistencies in tests on mental status and a normal EEG differentiates them from delirium.
Management:
1. The treatment is aimed at maintaining vital functions (B.P., temperature, hydration), correcting underlying medical disorders and reducing the disturbing psychological and behavioural symptoms.
2. The drugs which precipitate delirium (e.g., cimetidine, digoxin, aminophylline, centrally activing beta blockers, anticonvulsants etc.) should be avoided. The low dose of benzodiazepines especially lorazepam 1-2 mg. Clonazepam (0.5-2 mg) and newer drugs like alprazolam (0.5-1.5 mg) and buspirone and haloperidol (5-15 mg) are preferred in delirious patients (In hepatic failure, lorazepam is preferred).
3. Family should be provided with reassuring information about the illness and its complications.
2. Essay on Dementia:
Dementia is defined as a loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. In addition, there should be objective evidence of impairment in long-term memory. Dementia occurs in clear sensorium. If consciousness is clouded, delirium should be considered.
Epidemiology:
About 10-20 percent of all persons above age 65 has mild to moderate dementia, Alzheimer’s disease is the most common dementing disorder.
Etiology:
The common causes of Dementia are given in Table 13.2 (Mnemonic “Vindictive Mad”)
Alzheimer’s disease, accounts for 50 to 60 percent of all cases in the elderly.
(a) Alzheimer’s Disease (Dementia of Alzheimer’s Type or DAT):
Popularly known as “the disease of the century” it is the commonest degenerative cause of senile (over age 65) and presenile dementias (before age 65).
Epidemiology:
The exact prevalence of this disease in India is not known. In United States, it is estimated that the disease affects 1.5 to 2 million people and that at least 1 lac of them die every year.
Etiology:
The factors which are known to be associated with increased risk for Alzheimer’s disease are— family history, age, history of head trauma and Down’s syndrome.
(i) Genetic Factors:
The relatives of patients with either presenile or senile dementia have an increased risk of developing the disease.
(ii) Neurotransmitters:
The most consistent neurochemical defect described in Alzheimer’s disease is a striking decrease in brain choline acetyltransferase (CAT), the enzyme necessary for the synthesis of acetylcholine. These findings are greatest in all the cerebral cortex (especially hippocampus and amygdala). The decrease in CAT correlate with the increase in the severity of cognitive impairment.
(iii) Aluminium:
Aluminium plays some role in Alzheimer’s disease. In Alzheimer’s disease, aluminium levels are increased in areas of the brain with prominent neurofibrillary changes but not in areas with senile plaques alone. Aluminium also plays an important role in “Dialysis – Dementia “.
Pathology:
Neurofibrillary tangles (i.e., microscopic filamentous paired helical filaments). Senile plagues (i.e., clusters of degeneratives, nerve endings containing amyloid) and less prominently, gramulovacuolar changes are present in great numbers and over a greater expense.
Clinical Features:
The clinical features of dementia (senile or presenile) of Alzheimer’s type are described in Table 13.5.
Differential Diagnosis:
(i) Multiple cerebral infacts. Infectious diseases, alcohol abuse, metabolic disturbances, normal pressure hydrocephalus etc. Alzheimer’s disease is commonly insidious and steadily progressive, whereas multiinfarct dementia is abrupt in onset and progresses incrementally.
Similarly, the presence of focal localizing neurological signs and a history of cerebrovascular disease and hypertension increases the likelihood of multi-infarct dementia.
(ii) Normal process of aging.
(iii) Delirium.
(iv) Schizophrenia.
(v) Major Depression. (See Table 13.6).
(vi) Factitious disease with psychological symptoms.
Management:
(i) To Treat What is Treatable:
Treating the treatable focuses on the use of the appropriate psychopharmacological agents to relieve the noncognitive symptoms such as depression, agitation, hallucinations, delusions and sleep disturbance.
Modest results have been obtained with cholinesterase inhibitors (e.g., Rivastigmine, Tacrine, Donepezil, Metrifonate, Galantamine etc.) and acetylcholine precursors (e.g., lecithin, choline, arecholine). Cerebral vasodilators, stimulants, nootropics and neuropeptides are in the process of being scientifically evaluated.
To give support to patient as well as his caregiver important in the management of dementia.
Prognosis:
The mean duration of Alzheimer’s disease, from onset until death, is 7 years, but it varies widely.
(b) Multi-Infarct Dementia (MID):
It is the second most common form of dementia after Alzheimer’s disease. The essential feature of this dementia is a stepwise deterioration in intellectual functioning that early in the course leaves some intellectual functions relatively intact (Patchy deterioration).
Focal neurological signs and symptoms and evidence of significant cerebrovascular disease (judged to be etiologically related to the disturbance) are often present.
Epidemiology:
The prevalence of vascular dementia in contrast to Alzheimer’s disease is 10 percent versus 50 percent. The onset of MID is apparently earlier than that of primary degenerative dementia. It is apparently more common in men.
Clinical Picture:
There are two common distinct types of multi infarct dementia.
(i) Cortical dementia (Atherosclerotic or Hypertensive Disease of Large Arteries). It is marked by:
a) Recurrent transient ischaemic episodes and small strokes with gradual deterioration.
b) Neurological signs (small stepped gait, reflex asymmetries, transient Babinski, hemianopia, dysarthria etc.) are transiently quite prominent.
c) Nonspecific confusional episodes, apraxia (constructional), agnosia, aphasia, difficulties with topography, dressing and manual construction are common.
(ii) Subcortical (Hypertensive Small-Vessel Disease):
Also called “Lacunar syndrome” by Fisher, is due to bilaterally scattered small infarcts. There are episodes of strokes. It has steadily, deteriorating course. Pseudobulbar palsy is the neurological hallmark of this disorder, with stiff stumbling gait, bilateral long tract signs, dysarthria, blank facial expression and other brain stem and upper motor neurone signs.
Differential Diagnosis:
(i) Cortical MID:
See Table 13.7.
Treatment:
Primary prevention aims at removing risk factors (i.e., hyperlipidemia, smoking, obesity, diabetes mellitus and hypertension). Secondary prevention aims at early recognizing vascular inflammatory disorders.
The effects of a completed stroke cannot be reversed but transient ischaemic attacks can be treated with anticoagulation. Antiplatelet aggregation drugs can also be used to reduce incidence of strokes. Depression is a common complication (over 60%) and responds to antidepressants.
(c) Dementia Associated with Alcoholism:
The essential feature is dementia associated with prolonged and heavy ingestion of alcohol for which all other causes of dementia have been excluded. The mental changes of dementia should persist at least three weeks after the cessation of prolonged heavy drinking in order to make this diagnosis.
Epidemiology:
Alcoholism is the third commonest cause of dementia. In India, it is diagnosed much more frequently in men. Dementia occurs after 15-20 years of very heavy drinking.
Etiology and Pathology:
Vitamin B 1 (thiamine) deficiency leads to median thalamic, diencephalic, periventricular and upper brain stem lesions, with focal cell loss and small haemorrhages.
The frontal lobes are most commonly affected followed by parietal and temporal lobes.
Clinical Picture:
It may initially present as personality changes of frontal lobe type. Alcoholics manifest increasingly disregard for social conventions, lack foresight and planning, appear poorly motivated, labile, shallow or apathetic affect, increasing forgetfulness, slowing of cognitive processes and inability to remember important events herald the onset of dementia. Global deterioration may be due to chronic hepatic encephalopathy, respiratory failure due to smoking, metastatic and hormonal effects of neoplasm, anaemias (folate, iron and B12).
Differential Diagnosis:
(i) Alcohol Amnestic Disorder.
(ii) Other causes of Dementia.
Management:
Energetic medical treatment, detoxification and good nutrition can significantly improve the mental state of chronic alcoholics within a few weeks (3 to 4 weeks) after which there is more gradual improvement detectable at 6 months.
(d) Dementia Related to Acquired Immunodeficiency Syndrome (AIDS):
50-60% of patients with AIDS exhibit a triad of cognitive, behavioural and motor defects of sub cortical dementia called AIDS-Dementia complex (ADC) 25-30% patients have dementia as initial presentation. Dementia related to AIDS may be caused by direct HIV infection (by a lenti virus, a type of retro virus), by intracranial tumours and infections that arise as a result of immune impairment and by the indirect effects of systemic disease. Initial manifestations are apathy, psycho-motor retardation (mistaken for depression), memory loss and attentional impairment in the absence of aphasia or apraxia (mistaken for subcortical dementia).
Pathologically, there is diffuse cerebral atrophy with demyelination and spongiform changes in the centrum semiovale as well as neuronal loss and glial nodules. Diagnosis is by ELISA, Western Blot test, CT scan of brain (cortical atrophy 1-6 months before onset of cortical dementia), MRI (to also detect white matter lesion).
The neuropsychiatry complications of AIDS are:
Acute Complications:
1. Delirium.
2. Adjustment disorders
Chronic Complications:
1. AIDS Dementia
2. Organic Delusional Disorder
3. Organic Hallucinosis
4. Organic Affective Disorder
5. Organic Personality Disorder
3. Essay on Organic Amnestic Syndrome:
The important characteristic of this syndrome is impairment in short and long-term memory occurring in a normal state of consciousness.
Etiology:
Examples are head injury, surgical intervention, hypoxia, infarction in the territory of posterior cerebral arteries and herpes simplex encephalitis. The most common form of amnestic syndrome is that associated with thiamine deficiency secondary to chronic use of alcohol.
Clinical Picture:
The individual with an amnestic syndrome has both an ongoing inability to learn new and an inability to recall material that was known in the past.
There is also confabulation, apathy, lack of initiative and emotional blankness. ICD-10 diagnostic criteria include recent memory loss, no impairment of immediate retention and recall, attention, consciousness and global intellectual functioning and historical or objective evidence of brain disease or injury (especially with involvement of diencephalic or medial temporal areas.
Differential Diagnosis:
(i) Delirium.
(ii) Dementia.
(iii) Transient Global Amnesia (TGA)
(iv) Factitious disorder with psychological symptoms.
Management:
The most important step in management is the treatment of the underlying cause (e.g., thiamine deficiency). Supportive measures include the use of memory aids and environmental modifications. The underlying psychiatric illness (anxiety, depression etc.) should be treated with drugs.
4. Essay on Organic Delusional Disorder:
The essential feature is the presence of delusions that occur in a normal state of consciousness and that are due to a specific etiologic factor.
Etiology:
i. Amphetamines, cannabis, hallucinogens, alcohol (hallucinogens e.g., LSD may cause organic delusional disorder analogous to ‘flash back’ hallucinations).
ii. Temporal lobe epilepsy in which interictal organic delusional syndrome may appear.
iii. Huntington’s Chorea (paranoid features are prominent).
iv. Cerebral lesions (e.g., in nondominant hemisphere).
v. Multiple Sclerosis, SLE, Wilson’s disease.
Clinical Picture:
Persecutory delusions are the most common type. Depersonalization and hallucinations may be present but are not predominant. Mild cognitive impairment, perplexed, disheveled or eccentrically dressed, abnormalities of psychomotor activity or apathetic immobility.
Differential Diagnosis:
(i) Delirium.
(ii) Organic hallucinosis.
(iii) Organic mood syndrome.
(iv) Nonorganic psychotic disorders
Management:
The underlying cause needs to be identified and treated. The temporal lobe or diencephalic conditions may be treated with anticonvulsants especially carbamazepine. Neuroleptics may be used to control delusional disorder.
5. Essay on Organic Hallucinosis:
The essential feature is the presence of persistent or recurrent hallucinations that occur in a normal state of consciousness and that are attributable to a specific organic factor.
Etiology:
The most common cause of isolate hallucinations is an intoxication. Hallucinogens, Phencyclidine and Cannabis are the main offenders but therapeutic drugs e.g., digitalis, antiarrhythmic agents, cimetidine, high dose I.V. penicillin, and a variety of anticholinergic agents and other drugs e.g., anticonvulsants, neuroleptics or sedatives (antihistaminics, benzodiazepines) in over dosage may produce this.
The other causes may be sensory deprivation (as in blindness or deafness), seizure foci in the temporal and occipital lobes, tumours of occipital lobes, cerebrovascular accidents (infarcts) and classical migraine.
Clinical Picture:
Hallucinogens or blindness most often cause visual hallucinations whereas alcohol or deafness may produce auditory hallucinations. Delusions are not prominent and only related to the content or belief in the reality of hallucinations.
Accidents may occur in attempting to flee from frightening hallucinations.
Differential Diagnosis:
(i) Other Organic Disorders:
In Delirium, hallucinations, if present, occur with clouded consciousness. In dementia, hallucinations if present are associated with general loss of intellectual abilities. In Organic delusional syndrome, hallucinations are overshadowed by prominent delusions while in Organic mood syndrome, the major disturbance is of mood.
(ii) Schizophrenia and Affective Disorders.
(iii) Hypnagogic and Hypnopompic Hallucinations.
(iv) Charles Bonnet Syndrome:
It refers to visual pseudohallucinations occurring especially in elderly people with reduced visual activity.
Management:
It is better that safer to ‘talk the patient down’ than to treat with drugs. In persistent hallucinosis, empirical treatment with haloperidol (upto 5 mg per day) or carbamazepine (up to 200 mg per day) may be tried.
6. Essay on Organic Mood (Affective) Syndrome:
The characteristic feature of this syndrome is a disturbance in mood, resembling either a manic episode or a major depressive episode, that is due to a specific organic factor.
Etiology:
See Table 13.9
Clinical Picture:
The clinical phenomenology of this syndrome is same as that of a manic or major depressive episode. The severity of the disturbance may range from mild to severe.
Differential Diagnosis:
(i) Other organic disorders, delirium, dementia, organic hallucinosis, organic delusional syndrome.
(ii) Functional mood disorders.
(iii) Organic personality syndrome.
Management:
Successful treatment of organic mood syndromes is achieved by treatment of the underlying disease. If the mood syndromes cannot be reversed after the reversal of the organic factor, antidepressants and psychotherapy (in case of depression type) or a combination of lithium and antipsychotics (in case of manic type of syndrome) may be used.
7. Essay on Organic Personality Syndrome:
The characteristic feature is a marked change in personality that is due to a specific organic factor but that is not due to any other organic mental syndrome.
Etiology:
The most common causes are neoplasms (glioma or meningiomas of frontal lobes), head injury (including post-concussion syndrome), vascular disease, temporal lobe, epilepsy, neurosyphilis, multiple sclerosis, Huntington’s chorea, metabolic disorders, uremia, hypoxemia, endocrine disorders (thyroid and adrenocortical disease) and ingestion of certain substances.
Clinical Picture:
A common pattern is characterized by emotional liability and impairment in impulse control or social judgement, temper outbursts, belligerent, sudden bouts of crying with little or no provocation, sexual indiscretions. In temporal lobe epilepsy, there is marked humourless verbosity in both writing and speech, religiosity and occasionally exaggerated aggressiveness.
Mild cognitive impairment and irritability may be seen.
Differential Diagnosis:
(i) Dementia.
(ii) Organic mood disorder.
(iii) Attention deficit disorder.
(iv) Nonorganic disorders.
(v) Personality changes in epilepsy.
Management:
Disinhibited violent behaviour may respond to antipsychotics, carbamazepine, lithium or propranolol. If epilepsy is the underlying cause, carbamazepine may be used. Patients with head injury (frontal lobe syndrome) require supervision, structured environment and custodial care.
8. Essay on Organic Anxiety Syndrome:
It is characterized by prominent, recurrent, panic attacks, which are etiologically related to the organic factor but not occurring exclusively during the course of delirium.
Etiology:
The common causes of this syndrome are given in Table 13.10.
Differential Diagnosis:
(i) Other organic disorders. Delirium, organic delusional syndrome.
(ii) Anxiety neurosis.
(iii) Other nonorganic psychosis.
Management:
Removal of the primary cause and symptomatic treatment with drugs e.g., benzodiazepines, beta blockers may help in the managing the patients.
9. Essay on Organic Catatonic Disorder:
According to the ICD-10 the following features are required for the diagnosis of organic catatonic disorder, in addition to the general guidelines for the diagnosis of other organic mental disorders, described earlier:
1. Stupor (diminution or complete absence of spontaneous movement with partial or complete mutism, negativism, and rigid posturing);
2. Excitement (gross hypermotility with or without a tendency to assaultiveness);
3. Both (shifting rapidly and unpredictably from hypo- to hyperactivity).
Presence of the other catatonic phenomena increases the confidence in the diagnosis.
The catatonic symptoms and signs.
Etiology:
The etiology and management of organic catatonic disorder.
Management:
1. Treatment of the underlying cause, if amenable to treatment.
2. Symptomatic treatment with antipsychotics and electroconvulsive therapy (if needed).