Schizophrenia clinical presentation

The differential diagnosis of depression is organized along both symptomatic and causative lines. Symptomatically, major depression is differentiated from other disorders by its clinical presentation or its long-term history. This is, of course, the primary means of distinguishing psychiatric disorders in DSM-1V. The symptomatic differential of major depression includes other mood disorders such as dysthymic disorder and bipolar disorder, other disorders that frequently manifest depressed mood including schizoaffective disorder, schizophrenia, dementia, adjustment disorder, and post-traumatic stress disorder, and, finally, other nonpsychiatric conditions that resemble depression such as bereavement and medical illnesses like cancer or AIDS. 

Russell, A. (1994) The clinical presentation of childhood onset schizophrenia. Schizophr Bull 20 631-646. 

In the United States, the Research Diagnostic Criteria (RDC) (19) and the DSM-IV (8) both provide clear inclusion and exclusion criteria for a current episode ( Table 9-2). Evaluation of past episodes can be made using the Schedule for Affective Disorders and Schizophrenia—Lifetime Version (SADS-L) ( 20) or the Structured clinical Interview for DSM (21). In other countries, the Present State Exam (PSE) (22) can reliably distinguish mania from other disorders. Table 9-3 reviews the various clinical presentations of primary bipolar disorder and their related DSM-IV diagnoses ( 23) (see also Appendix A, Appendix G, and Appendix H). 

The clinical presentation of schizophrenia is characterized by positive symptoms, negative symptoms, and impairment in cognitive functioning. 

Schizophrenia is the most common functional psychosis, and there are as many clinical presentations of schizophrenia as there are individuals with the disorder. Despite numerous attempts to portray a stereotype in movies and on television, the stereotypic schizophrenic essentially does not exist. Moreover, schizophrenia does not mean... 

Edgell ET, Hamilton SH, Revicki DA, et al (1998). Costs of olanzapine treatment compared with haloperidol for schizophrenia results from a randomized clinical trial. Poster presented at the 21st CINP Congress, Glasgow, July 1998. 

Spannheimer A, Clouth J, Gregor KJ (1999). Pharmacoeconomic evaluation of the rrearmenr of schizophrenia in Germany a comparison of olanzapine, risperidone and haloperidol using a clinical decision model. Poster presented at the ISPOR Second Annual European Meeting, Edinburgh, November 1999. 

Circunstantial evidence directly implicating dopamine in the pathogenesis of duodenal ulcer in man is the unusual incidence of peptic ulcer disease in dopamine-deficient disorders. From purely descriptive clinical and epidemiologic studies we know that patients with Parkinson s disease, before the introduction of dopamine therapy, had an excess of ulcer disease (72). One report even comments on the curiosity that after initiation of L-DOPA administration the ulcer symptoms have virtually disappeared (72 ). On the other hand, less clearly, schizophrenia which is associated with dopamine excess and/or receptor hyperactivity is accompanied by virtual lack, or decreased prevalence, of peptic ulcer (73-76). Schizophrenia associated with ulcer disease has been viewed as a reportable curiosity in medical literature (75). At present, possibly because of the widespread therapeutic application of neuroleptics, the lack of peptic ulcer disease in schizophrenics is less striking than in the past. On the other hand, we recently observed in our autopsy series perforated duodenal ulcers in two schizophrenic patients who had been on large doses of haloperidol therapy (Szabo, unpublished observation). Thus, even in man, dopamine may indeed be implicated in the pathogenesis of duodenal ulcer disease. 

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