Schizophrenia and Acute Psychosis

Schizophrenia and Acute Psychosis



Manu Mathews, George E. Tesar, Omar Fattal, David J. Muzina



DEFINITION AND ETIOLOGY


Schizophrenia is a chronic and disabling neuropsychiatric illness possibly best characterized as a syndrome rather than as a single disease entity. The abnormal, often bizarre behavior that typifies schizophrenia is a product of disturbances in cognition, perception, and volition. Clinical manifestations are believed to result from incompletely understood dysregulation of frontotemporal and limbic neurocircuitry. The National Alliance for Mental Illness (NAMI), a patient- and family-oriented self-help group, has designated schizophrenia a brain disorder, emphasizing that schizophrenia is not simply a product of dysfunctional parenting or other psychosocial stressors. Studies have consistently shown, however, that both genetic and nongenetic factors play a role in the origin of schizophrenia.



PREVALENCE AND RISK FACTORS


The point prevalence of schizophrenia is 1% to 1.5%, a finding that has been fairly constant across time, cultures, races, and continents. It is equally prevalent in men and women. In the United States, about 2.5% of total annual health care expenditures are for schizophrenia. Globally, schizophrenia is a leading cause of disease burden and disability. The lifetime risk of suicide is nearly 7% compared with 14% to 15% for mood disorders such as major depression and bipolar disorder.1


The familial nature of the illness has long been recognized. Mounting evidence supports a strong genetic contribution, but genetic factors alone do not fully account for the variance in cause. As with other common illnesses such as hypertension, the risk of developing schizophrenia is a product of multiple genes interacting not only with one another but also with environmental factors. It is also possible that specific risk factors predict occurrence of specific schizophrenia subtypes.



Genetic Risk Factors


Accumulating evidence shows that genetic and neurodevelopmental factors are associated with greater susceptibility to schizophrenia. According to twin and adoption studies, up to 50% of identical (monozygotic) twins share a diagnosis of schizophrenia, compared with about 12% of nonidentical (dizygotic) twins. The strength of genetic factors varies across families, but approximately 10% of a patient’s first-degree relatives (parents, siblings, and children) are also schizophrenic, as are 50% of the children of two schizophrenic parents. Reports indicate suggestive linkage on chromosomes 1, 3, 5, and 11 and on the X chromosome.



Season of Birth


The birth rate of patients with schizophrenia is 5% to 8% higher worldwide than the birthrate of the general population in the winter and spring months. No proven explanation exists for this phenomenon. A greater likelihood of viral exposure during winter months has been proposed.



Early Developmental Insults


A comparatively high rate of peripartum infant hypoxia has been associated with structural brain abnormalities (e.g., increased ventricular and decreased hippocampal volumes) in schizophrenic patients and their nonschizophrenic siblings.



Other Factors


Population density, industrialization, emigration, and low socioeconomic status at birth have been proposed as possible influences on the development of schizophrenia.



PATHOPHYSIOLOGY AND NATURAL HISTORY


Gross inspection of the schizophrenic brain reveals no abnormalities. Modern neuroimaging techniques, however, including computed tomography (CT), magnetic resonance imaging (MRI), functional MRI (fMRI), and positron emission tomography (PET), demonstrate evidence of nonspecific structural and metabolic abnormalities in the frontotemporal cortices and periventricular limbic structures of the schizophrenic brain. Detailed postmortem analysis of protein profiles and metabolic patterns in the brains of schizophrenic patients point to mitochondrial dysfunction as a distinctive feature.2


Neural transmission has long been an object of investigation in schizophrenia. The first agents to demonstrate promise in the pharmacologic control of schizophrenia were recognized to have dopamine-blocking properties. Several neurotransmitter systems have been implicated, but the primary focus has been on dopamine and the brain structures that are high in its content (substantia nigra, ventral tegmentum, mesolimbic structures, and the tuberoinfindibular system). Five dopamine receptor subtypes (D1 through D5) have been identified. Blockade of the D2 receptor appears to have the greatest relevance to the antipsychotic efficacy as well as adverse effects of neuroleptic drugs. The site of D2-receptor blockade is also relevant to its benefits and adverse effects. Extrapyramidal symptoms can be attributed to D2-receptor blockade in the substantia nigra and ventral tegmentum, positive symptom suppression to D2 blockade in mesolimbic structures, and hyperprolactinemia to D2 blockade in the tuberoinfindibular structures (dopamine is a prolactin-inhibiting factor). The relationship to schizophrenia of serotonin, glutamate, gamma-aminobutyrate, neurotensin, and their relevant receptors is also under investigation.



SIGNS AND SYMPTOMS


The median age at onset for the first psychotic episode of schizophrenia is in the early to mid-20s for men and in the late 20s for women. A prodromal phase that lasts months to years can precede the first psychotic episode. Acute psychosis, the hallmark of the acute phase, follows the prodrome insidiously or occurs abruptly and sometimes explosively. The natural history without treatment (and sometimes with) is for symptoms to wax and wane, punctuated by recurrent episodes of acute psychosis. The pattern of symptoms can change over time, with progressive deterioration of function and cognition in some instances and progressive improvement of psychotic symptoms and function in others. Full recovery is uncommon, especially if the illness has been present for some years. Comorbid substance abuse is common, prolongs the illness, and contributes to treatment resistance.


The prodomal phase of schizophrenia is characterized by social avoidance, emotional flattening, eccentricity or magical thinking, idiosyncratic speech, and peculiarities of attitude and behavior that fail to meet criteria for a specific psychiatric illness. Prodromal symptoms that suggest social anxiety, panic, obsessive-compulsive or major depressive disorder, and antisocial behavior or substance misuse often lead to early misdiagnosis and unsuccessful treatment efforts.


Factor analysis has identified three main psychotic symptom dimensions in schizophrenia: positive, negative, and cognitive. The acute phase of the illness features a predominance of positive psychotic symptoms, whereas the chronic phase is typified by negative and cognitive symptoms. Unlike other types of psychosis, the positive symptoms of schizophrenia are complex and bizarre (i.e., having to do with unreal or unearthly events). Negative symptoms are believed to reflect neuroimaging evidence of reduced metabolic activity in the dorsolateral prefrontal cortex. Positive symptoms might represent abnormal temporal lobe activity. Characteristic features of positive, negative, and cognitive symptoms are outlined in Box 1.



Box 1 Schizophrenia Symptoms and Symptom Dimensions



Positive*



Hallucinations (typically auditory but also visual)

Delusions (paranoid delusions, nihilistic delusions, delusions of control)

Unusual behavior (stereotypies, mannerisms)


Negative†



Reduced emotional (affective‡) range

Diminished speech production (poverty of speech)

Loss of interest (anhedonia‡)

Loss of drive, initiative (apathy, abulia‡)

Indecisiveness (ambivalence‡)


Cognitive†



Poor attention

Working memory impairment

Formal thought disorder (tangential thinking, loose associations)§

Concrete thinking and impaired abstraction

Executive function deficits


* Typically bizarre (i.e., unreal, other-worldly, or impossible).


† Negative and cognitive symptoms of schizophrenia correlate with neuroimaging evidence of dorsolateral prefrontal cortex dysfunction.


‡ These are the 4 As of Bleuler.


§ Formal thought disorder (a disorder of the form of thought) is also considered a positive symptom.


Executive functions are the ability to initiate, regulate, plan, and sequence activities. The negative symptoms (apathy, indecision) can represent impaired executive functions.



DIAGNOSIS


Accurate diagnosis of schizophrenia is often challenging because symptoms are nonspecific and because progression to full illness is gradual. Relevant signs and symptoms must be present for at least 6 months before a diagnosis of schizophrenia can be made. Acute psychosis is a necessary but insufficient criterion for diagnosing schizophrenia. The diagnostic criteria for schizophrenia are symptomatic, functional, and time based, and they require exclusion of both medical and other psychiatric disorders that can mimic schizophrenia. Schizophrenia is largely a diagnosis of exclusion. The diagnostic criteria for schizophrenia specified by the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM IV-TR)2 are presented in Box 2.



Box 2 DSM IV-TR Criteria for the Diagnosis of Schizophrenia



Characteristic Symptoms


At least two of the following symptoms must be present, and each must be present for a significant portion of time during a 1-month period (or less if successfully treated):


• Delusions

• Hallucinations

• Disorganized speech (e.g., frequent derailment or incoherence)

• Grossly disorganized or catatonic behavior

• Negative symptoms (e.g., affective flattening, alogia, avolition)

Only one symptom is required if:


• Delusions are bizarre

• Hallucinations consist of a voice keeping up a running commentary on the person’s behavior or thoughts

• Two or more voices are conversing with each other


Social and Occupational Dysfunction


For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care are markedly below the level achieved before the onset


When the onset is in childhood or adolescence, failure to achieve expected level of interpersonal, academic, or occupational achievement



Duration


Continuous signs of the disturbance persist for at least 6 months


This 6-month period must include at least 1 month of characteristic symptoms (i.e., active-phase symptoms), or less than 1 month if successfully treated, and can include periods of prodromal or residual symptoms


During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or two or more characteristic symptoms present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences)



Schizoaffective and Mood Disorder Exclusion


Schizoaffective disorder and mood disorder with psychotic features have been ruled out because either


• No major depressive, manic, or mixed episodes have occurred concurrently with the active-phase symptoms

• Mood episodes have occurred during active-phase symptoms, but their total duration has been brief relative to the duration of the active and residual periods


Exclusion of Substance Use and General Medical Conditions


The disturbance is not due to the direct physiologic effects of a substance (e.g., drug of abuse, a medication)


The disturbance is not due to the direct physiologic effects of a general medical condition



Relation to a Pervasive Developmental Disorder


If there is a history of autistic disorder or another pervasive developmental disorder, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least 1 month (or less if successfully treated).


Schizophrenia also has subtypes (Box 3) defined exclusively by symptom predominance. Their validity remains controversial.



Box 3 Subtypes of Schizophrenia


Adapted from Markowitz JS, Brown CS, Moore TR: Atypical antipsychotics Part I: Pharmacology, pharmacokinetics and efficacy. Ann Pharmacotherapy 1999;33:73-85.



Paranoid


Preoccupation with one or more delusions or frequent auditory hallucinations


None of the following is prominent:


• Disorganized speech

• Disorganized or catatonic behavior

• Flat or inappropriate affect.


Disorganized


Disorganized speech and behavior and flat or inappropriate affect are prominent


Criteria are not met for catatonic type



Catatonic


Motor immobility, catalepsy, stupor


Excessive motor activity that appears to be purposeless


Extreme negativisim or mutism


Peculiarities of voluntary movement (inappropriate or bizarre posturing), stereotyped movements, prominent mannerisms, or prominent grimacing


Echolalia or echopraxia (repeating the examiner’s verbalizations or movements)



Undifferentiated


Characteristic symptoms (see Box 2) are present, but the criteria are not met for the other subtypes listed here



Residual


Absence of prominent delusions, hallucinations, disorganized speech, and grossly disorganized or catatonic behavior


Continuing evidence of negative symptoms (see Box 1) or two or more characteristic symptoms (see Box 2) in an attenuated form (e.g., odd beliefs, unusual perceptual experiences)

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Jul 18, 2017 | Posted by in GENERAL SURGERY | Comments Off on Schizophrenia and Acute Psychosis

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