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Organic psychiatric disorders are those mental disorders caused by a general physical illness or local brain disease which manifests with psychiatric symptoms. Many endocrine and metabolic disorders cause such mental diseases. For example, in thyrotoxicosis there are symptoms of anxiety, panic and sometimes psychosis. In hypothyroidism, one of the known symptoms is depression. Vitamin deficiency can cause mental changes. Liver failure may lead to hepatic encephalopathy, while kidney failure may cause renal encephalopathy. Suprarenal hormonal disturbances in Cushing's disease and Addison's disease are accompanied by psychological disturbances. Degenerative diseases of the brain such as dementias, amnesias, and Parkinson's disease presents with psychiatric symptoms.
Common Cause of Organic Psychiatric Disorders
Psychological symptoms are almost invariably present in thyrotoxicosis. Common symptoms include anxiety, hyperactivity, emotional lability without any preceding history of anxiety and no psychological precipitant. Less common symptoms are depression with agitation or apathy and early morning waking. Symptoms may persist after return to euthyroid state, and patients may require antidepressant therapy. Occasionally there is Euphoria. Rarely, thyrotoxic patients may present with acute organic confusion (in severe toxicity), or a schizophrenic reaction. Physical symptoms of thyrotoxicosis are weight loss in spite of good appetite, intolerance of hot weather, sleeping pulse more than 90/minute, and sometimes atrial fibrillation.
Basically, hypothyroid patients present with an organic mental syndrome with secondary psychological features depending upon personality type. It is most common in the elderly. When it occurs in infancy or childhood it may lead to mental handicap if it remains untreated and it is reversible if treated early. Common symptoms are memory impairment, dulled comprehension and myxoedema may lead to irreversible dementia. Depression with lethargy, or irritability can persist after return to euthyroid state and require antidepressant therapy. It is less common to find patients in coma which is often precipitated by infection, although there is high mortality when hypothermia also present ( Temperature less than 35'C).
Patients can be sometimes excessively suspicious, paranoid and may present with hallucinatory psychosis or mania. Physical features of hypothyroidism include sensitivity to cold, physical slowness, weight increase, non-pitting pretibial oedema, facial puffiness, hoarse voice, coarse dry skin, thinning of hair, carpal tunnel syndrome, angina (secondary to hypercholesterolaemia). Richard Asher coined the term 'myxoedema madness' to include a wide variety of psychiatric states.
See Wernicke's encephalopathy and Korsakoff's psychosis
There are distinctive symptoms with vitamin B12 deficiency such as memory deficits, poor concentration which are found in 25% of patients with Addisonian anaemia. These may precede neurological and haematological abnormality. It is important to screen for vitamin B12 deficiency in all undiagnosed organic brain syndromes, especially in the elderly, in patients with after surgery to the stomach (post-gastrectomy), and other intestinal diseases, as well as severe chronic dietary deficiency. Vitamin B12 may lead to progressive dementia in severe cases. Psychiatric symptoms are usually non-specific which may include affective disorders (such as anxiety, irritability, depression) in 20%. Folic acid deficiency is said to be more likely to cause affective disorder (56%).
Tryptophan deficient diets, neglect of diet in elderly may cause this deficiency. It may also secondary to chronic diarrhoea. There is initial depression and later confusion, delirium and dementia.
This is a range of neuro-psychiatric symptoms associated with hepatic insufficiency. Clinically there is chronic organic brain syndrome punctuated by episodic disorders of consciousness, with or without delirium and finally coma. In the early stages, the only finding may be a exaggeration of personality traits, anxiety depression or denial of illness, reversal of sleep rhythm, slowing of EEG, fluctuating degrees of concentration/awareness and constructional apraxia. In the later stages, there is confusion, inappropriate behaviour, delusional ideas, hallucinations or visual illusions (such as seeing things tiny or micropsia).
Hepatic coma may be heralded by stupor, fits, flapping tremor of hands, hypertonia and hyperreflexia with extensor plantar responses. Hepatic encephalopathy is due to metabolic changes secondary to liver cell failure. The precise metabolites involved are uncertain, although raised blood ammonia is usually found but its level does not correlate closely with severity of symptoms.
Toxic products of protein breakdown such as methionine and tryptophan metabolites entering systemic blood supply via new collateral extra-hepatic and intra-hepatic shunts are involved. Short chain fatty acids may also be toxic, as well as accumulation of neurotransmitters, originating from bacterial protein breakdown in gut. Coma may be precipitated by diuretics, high protein intake, presence of blood in gut, intercurrent infection, sedatives, phenothiazines, monoamine inhibitors and other antidepressants. Portal - systemic shunt (especially if surgically induced in treatment of portal hypertension) may be the cause of delusional and hallucinatory symptoms and central nervous damage (paraplegia, cerebellar and basal ganglion disease, epileptic fits).
Important to distinguish alcoholic delirium tremens from hepatic encephalopathy if it is only because use of sedatives can be fatal in the latter.
^ ^ Liver failure ^ Delirium Tremens ^ |Activity | Hypoactive apathetic state | Physically overactive| |Mood | May resemble depression | Vivid visual hallucinations, severe anxiety| |Tremors| Irregular flapping tremor | Tremor coarse, rhythmic | |EEG | progressive slowing | triphasic waves, with high amplitude |
This condition is due to excessive production of cortisol with variable amount of adrenal androgens. Adenoma or carcinoma of adrenal cortex is the cause in 20% of cases, and adrenal hyperplasia in 80% of cases. Psychological symptoms is evident in more than 50% off cases and they are more likely if there was a history of previous psychiatric difficulties. Symptoms improve with adequate treatment of the endocrine disorder.
Common symptoms are depression with anxiety or retardation, excessive fatigue, stupor, episodic acute excitement, anxiety, impotence, amenorrhoea, loss of libido. Severity of depression is not related to levels of circulating cortisol. It may be rapidly relieved when the tumour or the hyperplastic gland removed. Supra-renal tumours are less commonly associated with psychiatric symptoms than is hyperplasia.
Less common symptoms are paranoid delusions, or hallucinations. Elation may occur. Acute organic reactions may be manifested as a subjective complaint of memory impairment when objective findings are minimal.
This is a condition of chronic adreno-cortical insufficiency of cortisol, aldosterone, corticosterone and androgens. Primary atrophy is the cause in up to 50%. In the past tuberculosis was a more common cause. Psychological symptoms are present in all severe cases. Mild memory impairment is reported in 75% of cases. Organic type symptoms vary with the severity of underlying endocrine deficiency and hypoglycaemia. In Addisonian crisis, there may be delirium. Depression occurs in 25% of patients, apathy in 25% of them, irritability in up to 50%. It is rare to see other psychotic symptoms.
Psychological symptoms are more likely with high doses or prolonged treatment of ACTH and corticosteroid therapy. It is more common in people with history of previous psychiatric difficulties. Euphoria is the most common symptom (up to 70%). Depression is far less common (in contrast to Cushing's Disease). Irritability, tension. psychosis may occur (5%) in the form of mania, depression, stupor, disorientation, delusions, hallucinations, and catatonia. Psychological dependence with depression as a result of steroid withdrawal, sometimes occurs.
Chronic anterior pituitary failure occurs most commonly due to postpartum ischaemic necrosis. Early symptoms are loss of libido, and loss of pubic and axillary hair. The skin is pale and wrinkled. Weight loss is not a significant feature. Depression, apathy, self neglect, sensitivity to cold also occur. Sleepiness and memory impairment are some of the psychiatric symptoms with episodes of confusion. The patient may suffer delirium, with liability to become comatose and die in absence of endocrine replacement.
Pheochromocytoma is a rare tumour of adrenal gland tissue. It results in the release of too much epinephrine and norepinephrine, hormones that control heart rate, metabolism, and blood pressure . This condition may lead to episodic symptoms which mimic acute anxiety. Patients usually complain of severe headache, which is often precipitated by emotional arousal or physical exertion.
An insulinoma is a tumour in the pancreas that produces too much insulin. Symptoms include anxiety and behavioural changes; as well as confusion; convulsions; dizziness; headache; hunger; and loss of consciousness; Rapid heart rate. Behaviour may be episodic which may be out of character. Aggression, confusion and loss of consciousness occur in severe cases.
Clinical features may be due to uraemia, underlying disease process or secondary physical and psychological complications. Uraemic encephalopathy is essentially an organic brain syndrome. Psychological disturbance is found in 75% of patients who have blood urea of more than 250 mg%. At first the patient complains of fatigue, headache, poor concentration and later episodic confusion or delirium followed by coma.
Neurological symptoms of chronic renal failure involve myoclonic jerks, asterixis, (metabolic flap) usually at times of clouded consciousness, extra pyramidal rigidity, involuntary movements, neuropathy (painful paraesthesiae, restless legs syndrome), polymyositis (proximal limb weakness), epileptic fits (33%), and reversible amaurosis (temporary loss of vision). EEG degree of abnormality is correlated with level of consciousness. There is generalised slow wave activity, disorganisation, episodic semi-rhythmic slow waves, which may be triphasic in form, abnormal arousal responses. Spontaneous paroxysmal epileptiform abnormalities is also induced by photic stimulation, with or without convulsions. There is poor correlation with blood urea levels; probably other metabolic changes interact.
There are marked EEG changes during or after dialysis, especially if dialysis disequilibrium syndrome occur. The features are as above in uraemia. In chronic dementia dialysis, EEG shows diffuse slow waves, superimposed on rythmic high amplitude slow waves, triphasic waves, and complex discharges. This may precede clinical changes, and is made transiently worse by dialysis.
Psychological disturbance: Depression is one of the early features of uraemia which may mimic depression, but may develop secondarily. Anxiety and secondary defence mechanisms.
Neuropathological: There is some neuronal degeneration and loss. This may be overshadowed by vascular complications due to secondary disorders such as hypertension. Urea itself is not neurotoxic. Electrolyte and acid/base changes, especially when these are rapid, contribute to the brain pathology. Water intoxication and abnormal neurotransmitter metabolism are other factors.
High doses of penicillin may cause fits. Diuretics may cause hypokalaemia. Immunosuppressants and steroids may predispose to viral or fungal meningoencephalitis or reticuloendothelial tumours.
When carried out rapidly or there is severe initial metabolic abnormality, dialysis may lead to a 'disequilibrium syndrome' of headache, confusion, fits, coma. This may be due to cerebral oedema, or reactive hypoglycaemia may also be a factor. Dementia may also complicate dialysis. This form of dementia is usually progressive and fatal in few months, often with osteomalacia, multiple bone fractures, orofacial grimacing and fits. It appears to be unrelated to biochemical disturbance, and is not improved by further dialysis. It may be due to accumulation in brain of aluminium derived from water used in dialysis.
The ward environment may involve social isolation and sensory deprivation and these may heighten anxiety, accentuate confusion, precipitate delirium or paranoid reaction.
It is essential to arrange for a careful psychological screening of potential donors. A sudden irrational decision may be suspected especially when family coercion is present. It is important to exclude a donor who has markedly ambivalent relationship with recipient.
The characteristic clinical features of organic brain syndrome are tendency to show marked fluctuation in severity, which is usually worse at night, memory loss (most severe for recent events), impairment of consciousness (especially in acute forms), disorientation to time, place, or person and intellectual impairment in the form of defect of grasp of information and reasoning, as well as social disinhibition. Non-specific psychiatric symptoms include hallucinations (especially visual hallucination), mood disturbances (either emotional lability or depression), delusional ideas and focal neurological signs. Disorientation and clouding of consciousness predominates. There may also be anxiety, bewilderment, illusions, hallucinations (in delirium).
Organic brain syndrome may be due to metabolic, infective, toxic, traumatic, degenerative, or vascular causes. Alcohol or barbiturate withdrawal in habituated individuals and nutritional deficiency are some other causes. Wernicke's encephalopathy (thiamine deficiency) begins with global confusional state, drowsiness, inattention, disorientation, and failure of identification. Nystagmus and ocular palsies are frequent, and delirium tremens occurs in a third of cases. There is a need emergency for treatment with intramuscular thiamine 50 mg daily. Rapid recovery is possible, but may only be partial.
Dementia is a syndrome arising from cerebral disease, primarily causing impaired recent memory, with additional variable disturbance of intellect, abstract thinking, judgement, personality, affect and higher cortical functions (e.g. orientation, speech). It occurs in the absence of any alteration in consciousness, but may cause episodic confusion or delirium. The loss of intellectual abilities interferes with social or occupational functioning. Progressive selective deficits imply focal dysfunction. 3-5% of people over 65 years have severe dementia, similar proportion have a milder form. 80% over 80 years are not demented.
It is essential to have objective information from relatives, friends and work colleagues to ascertain change from premorbid function, duration, speed of onset and evidence of selective difficulty. Family history is essential in case of inherited disorders, such as Huntington's Chorea.
It is important to assess the degree of deficit as well as any possible causes, through:
A. Full general physical examination for evidence of systemic disease, such as metabolic or neoplastic disorder.
B. Neurological examination for focal cranial nerve or limb signs. It is relevant to look for apraxia .a defect of action inexplicable by simple motor or sensory loss which implies parietal lobe involvement.
C. Use of simple tests of mental function:
Where doubt remains and/or suspicion of selective deficits, then a detailed psychometric assessment may be required.
Cerebral atrophy is evident in 50% of cases.
constitute 50-70% of dementia patients over 65. There is also pre-senile types. There is early memory loss, dressing apraxia, disorientation, fits, and extrapyramidal signs which indicate neuronal loss. Histologically, there is argentophil plaques and neurofibrillary cell changes. There is marked involvement of parietal lobes.
is a rare cause of dementia which is a Mendelian dominant genetic disorder. There is characteristically early social disinhibition due to frontal lobe involvement, rigid egocentric attitude and focal neurological deficits are common, for example dysphasia. Memory loss is a late feature. Histologically, there is neuronal loss, and the presence of balloon-like Pick cells.
Multi-infarct dementia represent 10-30% of all cases of dementia. It affects thalamus, basal ganglia, brainstem and cerebrum. It can be coincidental with dementia from other causes. Depression is often marked initially.
The cortical atrophy in alcoholic dementia is in excess of the age effect.
This is charactrised by psychomotor retardation, ataxia and urinary incontinence. It has an insidious onset. There is ventricular enlargement with normal CSF pressure. It may occur after head injury, subarachnoid haemorrhage, intracranial surgery, cerebrovascular disease, meningo-encephalitis, with brainstem, glioma, third ventricular cyst, cerebellar tumour, aqueduct stenosis. In half of case, there is no obvious cause.
Improvement can follow introduction of intracerebral shunt. It is important to select and investigate patients needing care as significant morbidity is associated with treatment.
This is a dominant autosomal inheritance condition. It occurs in 5 out of 100 000 persons in the population. Some sporadic cases also occur due to mutation. Onset is usually between 30 and50 years of age. The dementia starts with depression or paranoid state initially. There is an increased family incidence of suicide, and antisocial behaviour. All children of an affected parent have 50% chance of developing the disease.
This together with normal pressure hydrocephalus and Huntington's chorea is sometimes called subcortical dementias' (see below).
Traumatic: The degree of dementia correlates well with duration of post-traumatic amnesia (the duration after injury before continuous memory recall is established).
Punch-drunk syndrome: Cerebral atrophy, which progresses until retirement from the ring, only occasionally afterwards. Cerebellar, pyramidal, extrapyramidal signs are characteristic with morbid jealousy and impotence.
Metabolic: Hypothyroidism, when chronic and severe. Hypoglycaemia (intermittent disordered behaviour, confusion or loss of consciousness more common than true dementia). Chronic renal dialysis, related to accumulation of aluminium from dialysis fluid. Hyperadrenalism, Cushing's syndrome. Hepatic failure. Addisonian anaemia.
Infective: Neurosyphilis: (general paralysis of the insane; G.P.l; tabo-paresis) may present with depression, grandiose paranoid psychosis (10%), social disinhibition. Human autoimmune deficiency syndrome (AIDS).
Impaired cerebral function can arise from subcortical lesions in several sites, but the clinical presentation tend to be similar : personality change, impaired memory (particularly retrieval), impaired information processing and ability to manipulate acquired knowledge. The patient may appear depressed, but in reality they lack initiative, are slow but antidepressants may cause further cognitive difficulty. The functions of language, calculation, and learning remain intact-unlike the cortical dementia.
Pathology: Changes affect subcortical grey or white matter or both. Causes include some frontal lobe tumours, the deterioration associated with progressive supra-nuclear palsy, Huntington's chorea, Parkinson's disease and other extra-pyramidal syndromes such as Wilson's disease, the spino~cerebellar degeneration:, and idiopathic calcification of the basal ganglia.
The differentiation of these syndromes from the cortical dementia is not always easy. Coincidental development of Alzheimer's disease has been suggested as the explanation for the dementia in Parkinson's disease. So far, no clear therapeutic advances have arisen from the subdivision.
Investigations Haemoglobin, White cell count, Erythrocyte sedimentation rate (indicates plasma viscosity), syphilis , and HIV antibodies in young at risk groups.
EEG can be useful, but normal age changes, as in dominant occipital frequency, may be confusing. It is important to exclude transient changes due to drug effects, toxic or metabolic disturbances. EEG slowing is most common in Alzheimer senile type, which is positively correlated with cognitive impairment. In early stage EEG may still be normal. It is of less value in multi-infarct type, unless infarcts are large or near surface, when local or focal EEG abnormalities may appear. Creutzfeldt-Jakob disease shows characteristic EEG changes of slow, disorganised record with periodic complex discharges. EEG may show abnormal sleep patterns in manifest senile dementia. Results are of greater diagnostic value in patient groups than in individual.
Evoked potentials. There is differential abnormality of the flash compared with pattern of visual evoked potentials reported in Alzheimer's disease. Somatosensory evoked potentials are more likely to be abnormal in Alzheimer's disease and multi-infarct dementia. As with EEGs, results of greater diagnostic value in patient groups than in the individual.
CT Scan Brain scan may show evidence of atrophy, either local or generalised. There is some degree of ventricular dilatation which correlates with severity of dementia. Combined CT scan and EEG with discriminant analysis can be valuable in Alzheimer's disease.
If necessary to investigate suspected neurological conditions using arteriography, isotope encephalography or in specialised centres MRI scan.
Differential diagnosis of dementia Depression may present with complaint of poor concentration and memory, (pseudo dementia). Schizophrenia simulates dementia through autistic behaviour, self-neglect. Hysterical amnesia may be global or selective for traumatic events. Chronic drug intoxication lead to slowness and poor concentration which may also occur in epileptic patients. In as many as 31% of patients presumed to be suffering from senile dementia the diagnosis is incorrect, being in fact a depressive illness or an acute confusional state.
The patient has defective recent memory as they can register memory but are only able of minimal recall. They may confabulate, confuse temporal sequence of events.
It is of sudden onset, usually with gradual but incomplete recovery. Bilateral hippocampal infarction due to occlusion of both posterior cerebral arteries, trauma affecting bilateral medial temporal lobes, subarachnoid haemorrhage, and carbon monoxide poisoning are some of the causes of amnesic syndrome. Amnesic syndrome may be traumatic, following a head injury.
Amnesic Syndrome of Sudden onset and Short duration Complex partial (temporal lobe) seizures. Post-Concussion. 'Transient global amnesia': This is a common form of amnesia in the elderly, which last a few hours, apparently with normal behaviour but only slight confusion. It is of vascular origin (probable transient ischaemia of hippocampal region due to platelet emboli). Transient Amnesia occur during any severe infection, e.g. severe pneumonia. Local infections of the brain in encephalitis or severe meningitis can present with amnesia. Metabolic changes, e.g. cerebral hypoxia, deficiency diseases, steroids, toxic substances such as carbon monoxide, glue-sniffing, metallic poisons and drugs, acute alcohol poisoning are other causes of amnesic syndrome.
Amnesia of subacute onset and varying degrees of recovery: Wernicke - Korsakoff syndrome, herpes simplex encephalitis, tuberculous or other granulomatous basal exudates.
Slowly progressive Amnesic Syndrome: Tumours involving floor and walls of third ventricle, early stage of Alzheimer's disease, other degenerative disorders with disproportionate involvement of the temporal lobes.
FURTHER READING Lishman,W.A. (1978) Organic Psychiatry. Oxford: Blackwell.