Schizophrenia Differential Diagnosis

Neurodegenerative disorders Rare neurodegenerative disorders occurring in late childhood and adolescence can mimic schizophrenia. The most important examples are Wilson’s disease (hepatolenticular degeneration) and metachromatic leucodystrophy.  These disorders usually involve significant extrapyramidal symptoms (e.g.  tremor,  dystonia and bradykinesia) or other motor abnormalities (e.g. unsteady gait) and a progressive loss of skills (dementia) that can aid the distinction from schizophrenia. Suspicion of a neurodegenerative disorder is one of the clearest indications for brain magnetic resonance imaging (MRI)  in child and adolescent onset psychoses. Children and adolescents with schizophrenia show relative grey matter reduction with white matter sparing. In contrast, metachromatic leucodystrophy is characterized by frontal and occipital white matter destruction and demyelination. In Wilson’s disease hypodense areas are seen in the basal ganglia, together with cortical atrophy and ventricular dilatation. The pathognomonic Kayser - Fleischer ring in Wilson’s disease begins as a greenish-brown crescent-shaped deposit in the cornea above the pupil (this is most easily seen during slit lamp examination).  In Wilson’s disease there is increased urinary copper excretion, and reduced serum copper and serum caeruloplasmin levels.  The biochemical marker for metachromatic leucodystrophy is reduced arylsulphatase-A (ASA) activity in white blood cells. This enzyme deficiency results in a deposition of excess sulphatides in many tissues including the central nervous system. Drug psychoses Recreational drug use is increasingly common among young people, so the co-occurrence of drug use and psychosis is to be expected. What is less certain is the nature of any causal connection. Psychotic symptoms can occur as a direct pharmacological effect of intoxication with stimulants (amphetamines, ecstasy and cocaine),  hallucinogens (lysergic acid diethylamide ‘LSD’,  psilocybin ‘magic mushrooms’  and mescaline) and cannabis (Poole & Brabbins 1996). The psychotic symptoms associated with drug intoxication are usually short-lived and resolve within a few days of abstinence from the drug. These drugs can have surprisingly long half-lives,  with cannaboids still measurable up to 6 weeks after a single dose. Psychotic symptoms in the form of ‘flashbacks’  can also occur after cessation from chronic cannabis and LSD abuse. These phenomena are similar to alcoholic hallucinosis and typically involve transient vivid auditory hallucinations occurring in clear consciousness. It is often assumed that there is a simple causal relationship between drug use and psychosis, with any evidence of drug use excluding the diagnosis of a functional psychosis.  However, drug use can also be a consequence of psychosis with patients using drugs to ‘treat’ their symptoms in the early stages of a psychotic relapse. Overall, there is very little evidence to invoke a separate entity of ‘drug-induced’ psychosis in cases where psychotic symptoms arise during intoxication but then persist after the drug is withdrawn (Poole & Brabbins 1996). Patients whose so-called ‘drug-induced’ psychoses last for more than 6 months appear to have more clear-cut schizophrenic symptoms,  a greater familial risk for psychosis and greater premorbid dysfunction (Tsuang et al. 1982). DSM-IV takes the sensible position that a functional psychosis should not be excluded unless there is compelling evidence that symptoms are entirely a result of drug use.

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