Psychiatric Annals

Neurological Diagnosis in Psychiatric Disease

Kenneth C Rickler, MD

Abstract

Advancements in clinical neuroscience have underscored the need for clinicians to consider and evaluate the possibility of neurological illness in patients presenting with psychiatric symptoms. Many psychiatrists feel uncomfortable with the medical concepts involved in neurological diagnosis; in a similar fashion, neurologists are often inadequately trained to deal with the complex psychosocial issues which surround organically-based behavioral disorders. The resurgence of interest in neuropsychiatrie disorders has heightened our awareness of these deficits and has led to the development of programs to train specialists in the field of organic behavior disorders. These programs will further the development of working relationships between neurologists and psychiatrists and lead to improved diagnostic and therapeutic skills.

The process of neurological diagnosis is a systematic attempt to examine anatomy in relation to function. The application of such a process to patients with psychiatric symptoms and/ or behavioral disorders presumes that simple and complex behaviors alike have an anatomical basis. A psychological level of experience does not occur in a vacuum, but rather is generated by neurophysiological processes in a unique environmental context. The environment and psychological processes in turn influence brain function. However, as Geschwind has noted, acceptance of the brain as the source of behavior may erroneously lead to the conclusion that all disorders of behavior are organic.1 Dysfunctional learning may be based on normal neurophysiological mechanisms and is often the major contributor to psychopathology. By contrast, organically-based psychiatric disorders involve disruption of the normal neurophysiological processes due to structural and/ or biochemical factors. This article will focus on selected aspects of organic mental disorders and the process of neurological diagnosis.

PSYCHIATRIC PRESENTATIONS OF UNRECOGNIZED NEUROLOGICAL ILLNESS

Traditional classifications of organic brain syndromes have focused on acute and chronic cognitive dysfunction. However, careful assessment reveals that neurologic illness may produce signs and/ or symptoms which are at times phenomenologically similar to psychiatric syndromes without obvious brain dysfunction. DSM III provides an updated comprehensive classification of organically-based psychopathology.2 The classification includes amnestic, delusional, hallucinatory, affective and personality syndromes as well as substance-induced disorders and the classic organically-based syndromes, delirium and dementia. Evidence of an etiologicallyrelated specific organic factor is required from history, physical examination, or laboratory tests in order to make a definitive diagnosis of an organic syndrome.

In the past, these phenomenological relationships have often been conveyed anecdotally. Case reports of frontal lobe meningioma producing the clinical picture of depression are notable for the lack of neurological signs early in the course.3 Structural disease of the basal forebrain involving frontal and temporal lobes has been described in relation to schizophreniform illness3 and personality disorders.4

A number of recent studies have examined the frequency of organically-based psychiatric illness in a systematic fashion. Koranyi's large outpatient study disclosed a significant percentage of unrecognized physical illness, which in 18% of the patients appeared as the causative factor for their psychiatric symptoms.5 Hall's outpatient study produced a lower figure of 9.1%,6 but his study of 100 inpatients disclosed that medical illness played a causative role in 46% of the patients.7 The incidence of primary neurological illness among medical causes of psychiatric disease ranged from 5.3%6 to 19%;5 tumors of the nervous system were often categorized separately. Hovey and Rickler evaluated 102 patients in an intermediate care psychiatric facility and noted that in 51% the major diagnosis was an organically-based psychiatric syndrome.8 Approximately one-half of the remaining 49% with a major functional diagnosis had evidence of other disease involving the nervous system.

These studies document the high frequency in which physical illness contributes to psychiatric symptoms. Although structural disease of the nervous system did not emerge as the leading cause…

Advancements in clinical neuroscience have underscored the need for clinicians to consider and evaluate the possibility of neurological illness in patients presenting with psychiatric symptoms. Many psychiatrists feel uncomfortable with the medical concepts involved in neurological diagnosis; in a similar fashion, neurologists are often inadequately trained to deal with the complex psychosocial issues which surround organically-based behavioral disorders. The resurgence of interest in neuropsychiatrie disorders has heightened our awareness of these deficits and has led to the development of programs to train specialists in the field of organic behavior disorders. These programs will further the development of working relationships between neurologists and psychiatrists and lead to improved diagnostic and therapeutic skills.

The process of neurological diagnosis is a systematic attempt to examine anatomy in relation to function. The application of such a process to patients with psychiatric symptoms and/ or behavioral disorders presumes that simple and complex behaviors alike have an anatomical basis. A psychological level of experience does not occur in a vacuum, but rather is generated by neurophysiological processes in a unique environmental context. The environment and psychological processes in turn influence brain function. However, as Geschwind has noted, acceptance of the brain as the source of behavior may erroneously lead to the conclusion that all disorders of behavior are organic.1 Dysfunctional learning may be based on normal neurophysiological mechanisms and is often the major contributor to psychopathology. By contrast, organically-based psychiatric disorders involve disruption of the normal neurophysiological processes due to structural and/ or biochemical factors. This article will focus on selected aspects of organic mental disorders and the process of neurological diagnosis.

PSYCHIATRIC PRESENTATIONS OF UNRECOGNIZED NEUROLOGICAL ILLNESS

Traditional classifications of organic brain syndromes have focused on acute and chronic cognitive dysfunction. However, careful assessment reveals that neurologic illness may produce signs and/ or symptoms which are at times phenomenologically similar to psychiatric syndromes without obvious brain dysfunction. DSM III provides an updated comprehensive classification of organically-based psychopathology.2 The classification includes amnestic, delusional, hallucinatory, affective and personality syndromes as well as substance-induced disorders and the classic organically-based syndromes, delirium and dementia. Evidence of an etiologicallyrelated specific organic factor is required from history, physical examination, or laboratory tests in order to make a definitive diagnosis of an organic syndrome.

In the past, these phenomenological relationships have often been conveyed anecdotally. Case reports of frontal lobe meningioma producing the clinical picture of depression are notable for the lack of neurological signs early in the course.3 Structural disease of the basal forebrain involving frontal and temporal lobes has been described in relation to schizophreniform illness3 and personality disorders.4

A number of recent studies have examined the frequency of organically-based psychiatric illness in a systematic fashion. Koranyi's large outpatient study disclosed a significant percentage of unrecognized physical illness, which in 18% of the patients appeared as the causative factor for their psychiatric symptoms.5 Hall's outpatient study produced a lower figure of 9.1%,6 but his study of 100 inpatients disclosed that medical illness played a causative role in 46% of the patients.7 The incidence of primary neurological illness among medical causes of psychiatric disease ranged from 5.3%6 to 19%;5 tumors of the nervous system were often categorized separately. Hovey and Rickler evaluated 102 patients in an intermediate care psychiatric facility and noted that in 51% the major diagnosis was an organically-based psychiatric syndrome.8 Approximately one-half of the remaining 49% with a major functional diagnosis had evidence of other disease involving the nervous system.

These studies document the high frequency in which physical illness contributes to psychiatric symptoms. Although structural disease of the nervous system did not emerge as the leading cause of psychopathology, it is clear that dysfunction of other organ systems may impact upon the nervous system and lead to psychiatric symptoms. A number of etiological mechanisms including neoplasm, trauma, infection, inflammation, intoxication, metabolic disturbance, vascular disease, degenerative processes and developmental abnormalities may act alone or in combination to produce psychopathology. Dementia and delirium remain the most common syndromes, but it is likely that an increased emphasis on thorough evaluation will disclose a higher percentage of contributory/ causal organic factors in illnesses characterized by psychosis or disturbances of affect. Slater and Glithero's follow-up study of patients with an initial diagnosis of hysteria serves as an important reminder of the frequent invalidity of this diagnosis.9 Fifty-six percent of 73 surviving patients evaluated an average of nine years after initial diagnosis had evidence of medical illness; in 30% an organic basis for their initial symptoms was determined.

Additional examples of unrecognized neurological illness associated with psychiatric symptoms include demyelinating disease, Wilson's disease, Parkinson's syndrome and herpes simplex encephalitis. Depression and/ or euphoria as well as subtle unrecognized cognitive deficits may characterize the early course of multiple sclerosis. Wilson's disease may produce disturbances of thinking for several years before motor symptoms are well-established; the latter may at times be mistaken for extrapyramidal side effects of neuroleptic medication. Depression may precede the onset of typical motor symptoms in Parkinson's disease. Patients presenting with herpes simplex encephalitis may be hospitalized in a psychiatric setting before seizures and progressive neurologic deficits declare the true nature of their illness. Thyroid disease may produce a variety of abnormal affective states and impair cognition; intoxication with a wide variety of poisons can produce subtle changes in mood, cognition and behavior. Lishman's treatise thoroughly catalogues the wide spectrum of organic mental disorders.10

NEUROLOGICAL SIGNS PRESENT IN PSYCHIATRIC DISORDERS

Psychiatric disorders without evidence of gross structural or metabolic brain disease may be accompanied by signs suggesting a mild degree of neurological dysfunction. The neurological examination may reveal minor impairments of coordination, higher cortical sensory function, patterns of motor activity and persistence, reflexes, gait, and multimodal sensory and sensory-motor integration. At times a subtle degree of "hard" neurological findings such as an upgoing toe may be noted. Mild abnormalities in the electroencephalogram and computed tomography may also be appreciated.

Although "soft" signs are most often described in relation to the attention deficit/ hyperkinetic syndrome, studies in schizophrenic patients have revealed a variety of minor non-localizing neurological and EEG abnormalities.11 Recent CAT scan data described by Weinberger and associates have revealed abnormalities in ventricular size and symmetry in schizophrenic patients.12

In contrast to the previously described syndromes with a well-defined organic basis, the assumption that "soft" signs implicate an organic contribution to the psychiatric symptomatology is more difficult to prove. A greater-than-chance association with various Psychopathologie entities and correlation with specific symptoms have been suggested.13 Jenkyn et al studied the predictive clinical significance of certain "soft" signs compared to the Hallstead-Reitan neuropsychological battery.14 Thirteen signs were found to correlate well with the test battery prediction of diffuse cerebral dysfunction, including abnormalities of gaze and visual tracking, limb placement and paratonia, and the suck, glabellar, and nuchocephalic reflexes. The etiological significance and prognostic value of "soft" signs with regard to associated psychopathology remain to be clarified by future studies.

BORDERLAND SYNDROMES

Intermittent explosive behavior, dissociative states and episodic psychosis exemplify complex neuropsychiatrie states in which the degree of organic contribution is difficult to determine. Dysfunction in the limbic system and other associated deep temporal lobe structures is presumed to be a common pathophysiological mechanism in these disorders.

While abnormal limbic discharges have been documented in association with explosive violent behavior, accurate dissection of characterological and psychological factors in these individuals remains difficult. Abnormal EEG activity between episodes of aggressive behavior may implicate intermittent and /or chronic dysfunction of limbic structures, but all such activity need not be negatively construed. It is highly likely that any given aggressive act is a multifactorial product.

Table

TABLE 1NEUROBEHAVIORAL HISTORY

TABLE 1

NEUROBEHAVIORAL HISTORY

Table

TABLE 2THE MENTAL STATUS EXAMINATION IN NEUROLOGY20

TABLE 2

THE MENTAL STATUS EXAMINATION IN NEUROLOGY20

Similar difficulties emerge when fugue-like episodes and depersonalized states are considered. Mayeux et al described prolonged episodes of aimless wandering in three patients with partial complex seizures and suggested that such behavior represents a prolonged post-ictal automatism.15 These behaviors terminated with adjustments in anticonvulsant therapy. Mesulam described a group of patients with multiple personality and/ or feelings of supernatural possession who demonstrated clinical and EEG manifestations suggestive of partial complex seizures.16 The temporal lobe has multimodal sensory and affective interconnections and its medial structures participate in memory consolidation. When viewed from the perspective of disordered information processing, the role of the temporal lobe in the production of symptoms involving altered consciousness, memory, perception and thinking becomes more apparent. Monroe has interpreted some recurrent schizophreniform episodes as reflecting an epileptoid process in the limbic structures, and has successfully treated some of these patients with anticonvulsants.17

NEUROLOGICAL DIAGNOSIS AND EVALUATION

A high index of suspicion for organic causes of mental symptoms is the most important step in diagnosis. While the subsequent evaluation requires knowledge and application of proper diagnostic strategies, the process must be set in motion by an appropriate level of concern. This is not to say that every patient with psychiatric symptoms demands thorough neuro behavioral assessment. Such a "reflex" approach could dilute the clinician's responsibility to become familiar with the patient's history and to formulate an initial diagnostic impression. A focus on potential organic problems should not lead the clinician away from significant dynamic material as well.

A thorough history, often requiring objective substantiation, is the next cornerstone for proper neurological evaluation of the psychiatric patient. The history should be oriented toward disclosing significant past or current organic processes and include questions regarding the topics listed in Table 1 . It may be necessary to request previous pediatric or school records as well as to consult relatives, neighbors, employers or friends for this information. Information collected in this careful and time-consuming fashion will assist in determining the nature and extent of the process or processes affecting the nervous system. A sudden onset of symptoms is more likely to suggest acute trauma, seizures, or vascular disease; a more gradual onset might be expected with neoplasm or late residuals from trauma. Metabolic disease may have an acute course as with hypoglycemia or present chronically with symptoms of hypothyroidism. Demyelinating disease and other inflammatory states may present with a pattern of relapse and remission.

The neurological examination involves the systematic assessment of functional neuroanatomy in an effort to localize the effects of etiological factors in caudal-rostral, anterior-posterior and right-left dimensions. Details of the physical neurological examination are beyond the current discussion and may be found in standard texts.18,19 The mental status examination in neurology is specialized toward disclosing information about the presence and extent of focal and/ or generalized cognitive dysfunction. The essentials of such an examination as proposed by Struband Black are listed in Table 2.20 The administration of the mental status examination to a cooperative patient requires approximately 20 minutes and provides valuable information about the anatomical basis of cognitive dysfunction.

Routine and specialized laboratory procedures augment the diagnostic process in neurology. Hall et al demonstrated the value of routine laboratory screening tests in the detection of organically-based psychiatric illness.7 Table 3 lists routine and specialized procedures which are helpful in the diagnosis of brain dysfunction. Several of these tests deserve comment. Multiple EEGs with sleep activation enhance the likelihood of detecting abnormalities. The use of nasopharyngeal (NP) leads may increase the yield but patients often find it difficult to sleep with NP leads, thus losing the value of sleep activation. Computerized tomography is underutilized in psychiatric diagnosis. However, as with any of the tests listed, abnormal findings must be correlated with the patient's symptoms/ behavior. Test results may be misleading as illustrated by patients with moderate cerebral atrophy who have no evidence of cognitive dysfunction. Among the special procedures listed, telemetry and positron emission tomography offer great promise for future assistance in the evaluation of patients presenting with psychiatric symptoms.

SUMMARY

Anecdotal experience and organized clinical studies have demonstrated the importance of neurological diagnosis in patients presenting with psychiatric symptoms. A variety of etiological factors may alter normal neurophysiological function to produce a wide spectrum of psychiatric illness, but a number of "borderland" syndromes remain difficult to characterize accurately from an organic viewpoint. Related "soft" signs may at times accompany psychiatric syndromes but are of uncertain etiological significance. Abnormal signs and laboratory data must be carefully correlated with the patient's symptoms. However, the absence of demonstrable neurologic abnormality does not necessarily exclude an organic etiology. An increased awareness of brain/ behavior relationships combined with a thorough history, comprehensive mental status examination, and appropriate utilization of laboratory investigations will result in improved diagnostic accuracy.

Table

TABLE 3LABORATORY INVESTIGATION

TABLE 3

LABORATORY INVESTIGATION

REFERENCES

1. Geschwind N: The borderland of neurology and psychiatry: Some common misconceptions, in Benson DF, Blumer D: Psychiatric Aspects of Neurologic Disease. New York, Grune and Stratton, 1 975.

2. Task Force on Nomenclature and Statistics: Diagnostic and Statistical Manuel. Third Edition (DSM-Hl); Washington, American Psychiatric Assn. 1980.

3. Blumer D, Benson DF: Personality changes with frontal and temporal lobe lesions, in Benson DF, Blumer D: Psychiatric Aspects of Neurologic Disease. New York. Grune and Stratton, I975.

4. Malamud N: Organic brain disease mistaken for psychiatric disorder. A clinical pathologic study, in Benson DF, Blumer D: Psychiatric Aspects of Neurologic Disease. New York, Grune and Stratton. 1 975.

5. Koranyi EK: Morbidity and rate of undiagnosed physical illnesses in a psychiatric clinic population. Arch Gen Psychiatry !979; 36:414-419.

6. Hall RC, et al: Physical illness presenting as psychiatric disease. Arch Gen Psychiatry 1978; 35:1315-1320.

7. Hall RC, et al: Physical illness manifesting as psychiatric disease. Arch Gen Psychiatry 1980; 37:989-995.

8. Hovey JE, Rickler KC: Neurobehavioral Evaluation and Diagnostic Study of 102 Patients in an "L" Facility. California State Départent of Mental Health. 1979.

9. Slater ET. Glithero E: A follow-up of patients diagnosed as suffering from "hysteria." y Psychosom Res 1965;9:9-13.

10. Lishman A: Organic Psychiatry. Boston. Blackwell Scientific Pubns Ine, 1978.

11. Pincus JH, Tucker GJ: Behavioral Neurology, ed 2. New York, Oxford Univ Press Inc. 1978.

12 Weinberger DR, Wyatt RJ: Structural brain abnormalities in chronic schizophrenia:. Computed tomography findings, in Baxter CF, Melnechek T (eds): Perspectives in Schizophrenia Research. New York, Raven Press Pubs, 1980, pp 29-38.

13. Tucker GJ: Sensorymotor disturbances in psychotics, in Bellak L: Psychiatric Aspects of Minimal Brain Dysfunction in Adults. New York, Grune and Stratton. 1979.

14. Jenkyn LR, et al: Clinical signs in diffuse cerebral dysfunction. Neurol Neurosurg Psychiatry 1977: 40:956-966.

15. Mayeux R et al: Poriomania. Neurology 1979; 29:1616-1619.

16. Mesulam M: Dissociative states with abnormal temporal lobe EEG. Arch Neurol 1981; 38:176-181.

17. Monroe RR: Episodic Behavioral Disorders. Cambridge, Massachusetts, Harvard Univ Press, 1970.

18. Denny-Brown D: Handbook of Neurological Examination and Case Recording. Cambridge, Massachusetts, Harvard Univ Press, 1965.

19. DeJ ong RN: The Neurological Examination, ed 3. New York, Harper & Row Pubs Inc. 1967.

20. Strub RL. Black FW: The Mental Status Examination in Neurology. Philadelphia, FA Davis. 1977.

TABLE 1

NEUROBEHAVIORAL HISTORY

TABLE 2

THE MENTAL STATUS EXAMINATION IN NEUROLOGY20

TABLE 3

LABORATORY INVESTIGATION

10.3928/0048-5713-19830501-05

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