Organic Psychiatric Disorders
A. ENDOCRINE, METABOLIC AND DEFICIENCY DISORDERS
Psychological symptoms are almost invariably present.
Common.
Anxiety, hyperactivity, emotional lability.
Often no preceding history of anxiety
May be no psychological precipitants.
Less common.
Depression with agitation or apathy, early morning waking.
May persist after return to euthyroid state, and require antidepressant therapy.
Euphoria or 'hypomanic veneer'.
Rare.
Acute organic confusion (in severe toxicity),
schizophrenic reaction.
Physical
Weight loss in spite of good appetite,
intolerance of hot weather,
sleeping pulse more than 90/minute,
atrial fibrillation.
Basically an organic mental syndrome
with secondary psychological features depending upon personality type.
Most common in the elderly. When it occurs in infancy or childhood it may
lead to mental handicap if it remains untreated; it is reversible if treated
early.
Common.
Memory impairment, dulled comprehension.
May lead to irreversible dementia.
Depression with lethargy, irritability
(may present in this way): can persist after return to euthyroid state
and require antidepressant therapy.
Less common.
Coma: often precipitated by infection, high mortality when hypothermia also present. (< 35'C).
Excessive suspiciousness, paranoid and hallucinatory psychosis.
Mania.
Physical features.
Cold sensitivity,
physical slowness,
weight increase,
non-pitting oedema (pretibial),
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.
VITAMIN B1 (thiamine) DEFICIENCY
See Wernicke's encephalopathy
and Korsakoff's psychosis
VITAMIN B 12 DEFICIENCY
Distinctive.
Memory deficits, poor concentration:
found in 25% of patients with Addisonian anaemia. May precede neurological
and haematological abnormality.
Screen for B12 deficiency: all undiagnosed organic brain syndromes, especially in elderly, postgastrectomy, other intestinal diseases, severe chronic dietary deficiency.
May be progressive dementia in
severe cases.
Non-specific.
Affective disorder (anxiety, irritability, depression) in 20%.
Folic acid deficiency is said
to be more likely to cause affective disorder (56%).
NICOTINIC ACID DEFICIENCY (Pellagra)
Tryptophan deficient diets.
Neglect of diet in elderly.
Secondary to chronic diarrhoea.
Initial depression.
Later confusion, delirium and dementia.
A range of neuro psychiatric
disorders associated with hepatic insufficiency.
Clinical features
Chronic organic brain syndrome
punctuated by episodic disorders of consciousness, with or without delirium
and finally coma.
In early stages:
- exaggeration of personality traits
hepatic coma (may be heralded by stupor, fits, flapping tremor of hands, hypertonia and hyper-reflexia, extensor plantar responses)
Differential diagnosis
Important to distinguish alcoholic
delirium tremens from hepatic encephalopathy if only because sedatives
can be fatal in latter.
Liver failureDTs
Hypoactive apathetic state Physically overactive
May resemble depression Vivid visual hallucinations, severe anxiety
Irregular flapping tremor Tremor coarse, rhythmic
may occur
EEG: progressive slowing
with high amplitude
triphasic waves
Due to excess production of cortisol with variable amount of adrenal androgens.
Adenoma or carcinoma of adrenal cortex (20%)
adrenal hyperplasia(80%).
Psychological symptoms in >50%: more likely
history o previous psychiatric
difficulties, improve with adequate treatment of endocrine disorder.
Common. Depression with anxiety or retardation, excessive fatigue, stupor, episodic acute excitement, anxiety, impotence, amenorrhoea, loss of libido. Severity of depression not related to levels of circulating cortisol: it may be rapidly relieved when tumour or hyperplastic gland removed. Tumour less commonly associated with psychiatric symptoms than is hyperplasia.
Less common. Paranoid delusions,hallucinations. Elation,
Acute organic reactions: may be subjective complaint o memory Impairment when objective findings minimal.
Chronic adrenocortical
insufficiency of cortisol, aldosterone, corticosterone and androgens. Primary
atrophy (up to 50%). In the past tuberculosis more common. Psychological
symptoms present in all severe cases. Mild memory impairment (75%). Organic
type symptoms vary with severity of underlying endocrine deficiency and
hypoglycaemia: in crisis there may be delirium. Depression (25%), apathy
(25%), irritability (up to 50%). Rare to see other psychotic symptoms.
ACTH AND CORTICOSTEROID THERAPY
Psychological symptoms
more likely with high doses or prolonged treatment, or history of previous
psychiatric diffleulties. Euphoria (up to 70%). Depression far less common
(contrast Cushing's Disease). Irritability, tension. PS chosis (5%): mania,
depression, stupor, disorientation, delusions, hallucinations, catatonia.
Psychological dependence with depression as a result of steroid withdrawal,
sometimes occurs.
HYPOPITUITARISM
Chronic anterior pituitary
failure. Most commonly due to postpartum ischaemic necrosis. Early loss
of libido, pubic and axillary hair. Skin pale, wrinkled. Weight loss not
a significant feature. Depression, apathy, self neglect. Sensitivity to
cold. Sleepy. Memory impairment. Episodes of confusion. delirium, liability
to become comatose and die in absence of endocrine replacement.
PHAEOCHROMOCYTOMA
May lead to episodic symptoms
which mimic acute anxiety. Usually severe headache. Often precipitated
bv emotional arousal or physical exertion.
INSULINOMA
Episodic which may be out of
character. aggression, confusion and loss of consciousness in severe cases.
FURTHER READING
Lishman,W.A. (1978) Organic Psychiatry. Oxford: Blackwell.
Clinical features May be due to
- uraemia
Neurological disorder
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%),
reversible amaurosis.
EEG changes
Degree of abnormality correlated
with level of consciousness. Generalised slow wave activity, disorganisation,
episodic semi-rhythmic slow waves, may be triphasiforms, abnormal arousal
responses. Spontaneous paroxysmal epileptiforabnormalities also induced
by photic stimulation, with or without convulsions. Poor correlation with
blood urea levels; other metabolic changes interact.
Dialysis: marked EEG changes
during or after, especially if dialysis disequilibrium syndrome, features
as above in uraemia. Chronic dementia analysis: diffuse slow waves, superimpose
rythmic high amplitude slow waves, triphasic waves, complex discharges.
May precede clinical change, and made transiently worse by dialysis.
Psychological disturbance
Depression: early features of uraemia may mimic this, but may develop secondarily.
Anxiety
Secondary defence mechanisms
Aetiology
Neuropathological. Some
neuronal degeneration and loss. May be overshadowed by vascular complications
due to secondary disorders such as hypertension. Urea itself not neurotoxic.
Electrolyte and acid/base
changes. Especially when these are rapid.
Water intoxication
Abnormal neurotransmitter
metabolism
Wernicke's encephalopathy:
thiamine
deficiency.
Iatrogenic. High doses
of penicillin may cause fits. Diuretics may cause hypokalaemia. Immunosuppressants
and steroids may predispose to viral or fungal meningoencephalitis or reticuloendothelial
tumours.
Effects of dialysis
When carried out rapidly or there is severe initial metabolic abnormality, then 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. Usually progressive and fatal in few months, often with osteomalacia,
multiple bone fractures, orofacial grimacing and fits. Appears to be unrelated
to biochemical disturbance, and not improved by further dialysis. May be
due to accumulation in brain of aluminium derived from water used in dialysis.
Hospital ward regimes
May involve social isolation
and sensorv deprivation. These may heighten anxiety, accentuate confusion,
precipitate delirium or paranoid reaction.
Renal transplantation donors
Careful psychological screening of potential donors.
Sudden irrational decision suspect especially when family coercion present.
Exclude donor who has markedly ambivalent relationship with recipient
ORRANIC BRAIN SYNDROMES
Causes
Metabolic, infective, toxic, traumatic, degenerative, vascular. Alcohol or barbiturate withdrawal in habituated individuals, nutritional deficiency. Wernicke's encephalopathy (thiamine deficiency), begins with global confusional state, drowsiness, inattention, disorientation, failure of identification. Nystagmus and ocular palsies frequent, and delirium tremens in a third. Emergency
need for treatment with intramuscular thiamine 50 mg daily. Rapid recovery 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 milder effect. 80% over 80 years are not demented.
History
Essential to have objective information
from relatives, friends and work cal leagues to ascertain change from premorbid
function, duration, speed of onset and evidence of selective difficulty.
Family history in case of inherited disorders, e.g. Huntington's Chorea.
Examination
To assess degree of deficit as well as possible causes.
a) Full general physical for evidence of systemic disease, e.g. metabolic or neoplastic.
b) Neurological for focal cranial nerve or limb signs. N.B. Look for apraxia - a defect of action inexplicable by simple motor or sensory loss - implies parietal lobe involvement.
c) Simple tests of mental function:
1. Language:
dysgraphia - writing disorder.
Cerebrovascular disease Multi-infarct
dementia (10-30%). Affects thalamus, basal ganglia, brainstem and cerebrum.
Can be coincidental with dementia from other causes. Depression often marked
initially.
Alcoholic dementia (5-10%).
Cortical atrophy in excess of age effect. 5-10%). Cortical atrophy in excess
of age effect.
Normal pressure hydrocephalus (Adams syndrome) (6%). Psychomotor retardation, ataxia and urinary incontinence. Insidious onset, ventricular enlargement, normal CSF pressure. May occur after head injury, subarachnoid haemorrhage, intracranial surgery, cerebrovascular disease, meningo~ncephalifis, with brainstem, glioma, third ventricular cyst, cerebellar tumour, aqueduct stenosis.
In half there is no obvious cause.
Important because improvement
can follow introduction of intracerebral shunt. Selection and investigation
of patients needs care as significant morbidity associated with treatment.
Huntington's chorea (3%).
Dominant autosomal inheritance. Incidence 5/100 000. Some sporadic cases
occur (mutation). Onset 30-50 years of age. May be depression or paranoid
state initially. Increased family incidence of suicide, antisocial behaviour.
All children of an affected parent have 50% chance of developing the disease.
Parkinson's disease. This together with normal pressure hydrocephalus and Huntington's chorea sometimes called
'subcortical dementias' (see
below).
Chronic drug intoxication
Miscellaneous diseases (7-10%).
- Traumatic. Degree of dementia correlates well with duration of post-traumatic amnesia (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, morbid jealousy, impotence.
- Metabolic. Hypothyroidism, when chronic and severe. Hypoglycaemia (intermittent disordered behaviour, confusion or loss of consciousness more common tha true dementia). Chronic renal dialysis, related to accumulation of aluminiumfrom 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).
- Hypoxic. CoaI.gas poisoning: beware late deterioration after 10 days.
- Other neurological disorders. There may be inappropriate euphoria in multiple sclerosis; frontal lobe tumours can cause disinhibited behaviour. Dementia with Parkinson's disease, with cerebellar atrophy e.g. Ramsay-Hunt syndrome, neurosyphilis, Creutrfeldt-Jakob disease, chronic undetected subdural haematoma.
Investigations
Hb, WBC, ESR (or plasma viscosity), W. R., and HIV antibodies in young at risk groups.
EEG
Can be useful. but normal age changes, e.g. in dominant occipital frequency, may be confusing. Must exclude transient changes due to drug effects, toxic or metabolic disturbances. EEG slowing most common in Alzheimer senile type, positively correlated with cognitive impairment. In early stage may still be normal. Less value in multi-infarct type, unless infarcts large or near surface, when local or focal EEG abnormalities. Creutzfeldt.Jakob disease: slow, disorganised record with periodic complex discharges. May be abnormal sleep patterns in manifest senile dementia.
Results are of greater diagnostic
value in patient groups than in individual.
Evoked potentials.
Differential abnormality of the
flash compared with pattern visual evoked potentials reported in Alzheimer's
disease. Somatosensory evoked potentials more likely to be abnormal in
Aliheimer's disease and multi-infarct dementia. As with EEGs, results of
greater diagnostic value in patient groups than in the individual.
CTscan
Evidence of atrophy, local or generalised. Degree of ventricular dilatation 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: 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: global or selective for traumatic events. Chronic drug intoxication: slow, poor concentration (may 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 (Ron 1979).
Drug treatment
'Cerebral metabolic enhancers',
centrally acting vasodilators, drugs acting at various sites in the cholinergic
systern, and a miscellaneous group including opioid and adrenergic antagonists,
as well as anticonvulsants are all currently suggested as treatment regimens
in dementia but have not been shown to have sufficiently sustained benefits
to justify their general use outside a research setting.
Top
THE
AMNESIC SYNDROMES
Recent memory defect (can register
memory but only minimal recall present). May confabulate, confuse temporal
sequence of events.
Sudden onset, usually with
gradual but incomplete recovery' Bilateral hippocampal infarction (occlusion
both posterior cerebral arteries), trauma affecting bilateral medial temporal
lobes, subarachnoid haemorrhage, carbon monoxide poisoning. Traumatic,
following a head injury (see separate section, p.33-35).
Sudden onset, short duration
Complex partial (temporal lobe)
seizures. Post~oncussion. 'Transient global amnesia'1 common
in the elderly, lasts a few hours: apparently normal behaviour but slight
confusion of vascular origin (probable transient ischaemia of hippocampal
region due to platelet emboli). Transient during any severe infection,
e.g. severe pneumonia. Local infections: encephalitis, severe meningitis.
Metabolic changes, e.g. cerebral hypoxia, deficiency diseases, steroids,
toxic substances such as carbon monoxide, glue-sniffing, metallic poisons
and drugs, acute alcohol poisoning.
Subacute onset, varying
degrees of recovery Wernicke - Korsakoff syndrome, herpes simplex encephalitis,
tuberculous or other granulomatous basal exudates.
Slowly progressive
Tumours involving floor and walls of third ventricle, early stage of
Alzheimer's disease, other degenerative disorders with
disproportionate involvement
of the temporal lobes.