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Essentials of the Neurological Evaluation

1.1 Introduction

The evaluation of the psychiatric patient is enhanced by the use of a general systems approach. Biological, psychological, and sociological systems variables should be identified and their interaction assessed. A central part of this evaluation concerns the role that the nervous system plays in the expression of mental and behavioural disorders. Our understanding of "functional" psychiatric illness has been irrevocably influenced by the prevalence in our patients of causative or contributory central nervous system (CNS) dysfunction.

...As a prerequisite, the examiner must have an understanding of the structure and function of the nervous system. For example, a systemic illness that eventually influences the central nervous system may present initially with a peripheral nervous system sign and a nonspecific mental state change. This change in behaviour may be ignored, whereas in actual fact it represents a focal central neurological finding.
In addition to the division of the nervous system into central and peripheral anatomic components, a functional division into voluntary (skeletal) and involuntary (autonomic) can be made. Traditionally, conversion syndrome diagnoses have been based on functional voluntary nervous system symptoms, sometimes ignoring the subtle neurological signs that would confirm the presence of central nervous system disease.

Multiple sclerosis has been the "great masquerader" for functional psychiatric illness and is commonly misdiagnosed as conversion reaction. Similarly, involuntary nervous system dysfunction may not necessarily indicate parasympathetic or sympathetic neuropathology because we now know that both classical and operant conditioning paradigms affect autonomic nervous system function. Thus, involuntary autonomic signs can exist as a result of a learned reaction rather than tissue dysfunction. Autonomic nervous system activity is constantly monitored and interpreted by higher cortical centers... especially those in the temporal lobe, modulate and affect production and consequently shape the organism's behavioural response...

2.2.6 Demyelinating Disease: Multiple Sclerosis

Clinical lore has it that one of the most difficult differential diagnoses in neurology or psychiatry is between the diagnosis of multiple sclerosis and hysteria/conversion syndromes. The diverse effects of multiple, widespread, and apparently unrelated demyelination of the central nervous system produce a puzzling clinical picture that is further obscured by the recurrent remitting nature of the disease. Psychopathological complaints may be more impressive than motor or sensory complaints when the former include affective dyscontrol (e.g. hypomania, depression, temper outburts, and labile emotionality), psychosis, or nonspecific personality change.

The linkage of cobalamin and folate deficiency to psychiatric illness has been studied and debated since these vitamins were first discovered in the 1940s. The clinical relevance of these deficiencies remains the subject of investigation and scholarly discussion. This article reviews case reports and studies derived from a MEDLINE search for English-language articles related to folate, cobalamin, and psychiatric illness. Emphasis is given to clinical research and recent developments. Preclinical evidence for direct effects of folate and cobalamin on brain functioning is compelling, and numerous associations of their deficiencies to psychiatric illness are evident. These vitamin deficiencies may typically present initially with psychiatric symptoms, but any direct causal relationship to specific neuropsychiatric illnesses are not well defined. The relationship of these vitamins in dementia is significant, but they may only rarely be a cause of truly reversible dementia. Folate deficiency appears most tightly connected with depressive disorders, and cobalamin deficiency with psychosis. Contrary to intuition, vitamin deficiencies appear to occur infrequently with eating disorders. Other diagnoses have been investigated much less extensively. The diagnosis and management of these deficiencies in the context of neuropsychiatric illness is still a matter of discussion. The quality of clinical research in this area is improving, but there are many unanswered questions that affect clinical practice. Clinicians should remain vigilant to the possibility of deficiencies of folate and cobalamin in diverse psychiatric populations. Normal hematological indices do not rule out the deficiencies. Further study is needed to refine the detection and clinical management of these vitamin deficiencies in psychiatric populations.

My husband had signs of depression and anxiety for years before his MS diagnosis and beginning Copaxone, so we knew his was pre-existing.