Raymond Faber

Suicide in Neurological Disorders

Accessible online at: www.karger.com/ned Suicide is an avoidable tragedy. The clinicians’ interest and vigilance are the most potent available deterrents. Individuals in high-risk groups can be identified, and practical, effective interventions are available. A number of neurological disorders have been identified among risk factors for suicide, so it behooves neurologists to be mindful of these conditions and to have a general awareness of suicide potential and management options. In the accompanying article, Fredrikson et al. [1] confirm an elevated risk of suicide in patients with multiple sclerosis. The twofold increase in standardized mortality ratio was comparable with that found in an earlier Danish study [2]. The methods by Fredrikson et al. [1] were excellent, yet in interpreting their work, it must be remembered that their lengthy data collection period was mainly in a period of relative therapeutic nihilism, before s-interferon became available. Now that effective treatments for multiple sclerosis are available, the hopelessness of sufferers may be mitigated. The highest risk of suicide was amongst younger males in the early years after diagnosis. Male gender is a very well recognized risk factor for suicide, partially because of its association with alcohol abuse. Other neurological disorders also confer an increased risk of suicide [3]. Stroke increases suicide risk [4]. Poststroke depression is often the soil from which suicide ideation emerges. The presence of persistent physical and cognitive impairments also contributes to suicide risk. Particular mention needs to be made of right frontal lobe strokes, which cause a motor aprosodia. In such instances, though these patients may complain of significant dysphoria, hopelessness, and suicide ideation, their inability to convey emotionality and feeling can cause disbelief in observers who tend to underestimate the severity of such utterances [5]. Huntington’s disease carries an increased risk of suicide. In his original article, Huntington [6] stated ‘the tendency to insanity and sometimes to that form of insanity which leads to suicide is marked’. Huntington patients are at risk for a plethora of psychiatric disturbances including mood disorders, psychosis, and personality disorders [7]. Even asymptomatic individuals at risk for Huntington’s disease need to be carefully screened for suicide ideation, before and after predictive genetic testing is carried out [8]. Epilepsy also carries an increased risk of suicide [9]. In addition to comorbid psychopathology, other factors increasing risk include higher seizure frequency and the need for multiple antiepileptic medications [10]. Temporal lobe foci may be a risk factor, but it may be their association with psychopathology that leads to suicide risk. Occasionally effective treatment results in the phenomenon of forced normalization wherein seizures are controlled but mental status deteriorates, sometimes dramatically so [11]. Vigabatrin has been associated with depression, but most newer antiepileptic drugs are either psychiatrically benign or even beneficial, i.e. divalproex and

Depression and spinal cord injury.

An especially pertinent fi nding from this longitudinal study is the identifi cation of when depression is most likely to occur after SCI. The greatest risk is during the initial hospitalization when over half of all those ultimately given the diagnosis of depression were diagnosed. The risk lessens but is still signifi cant in the fi rst 2 years after SCI. Beyond 2 years, the risk appears about equal with the general population. Multivariate analysis revealed three factors associated with depression. These were the diagnosis of an anxiety disorder, some permanent paralysis, and prior history of depression. However, none of these were particularly sensitive or specifi c and are less important than an overall high index of suspicion for depression following SCI. Any clinician who cares for patients with SCI can readily initiate treatment of depression. Recognition is paramount and every person with SCI should be screened and monitored for depression. I prefer an individualized approach to diagnosis rather than having patients fi ll out a self-rating questionnaire. Sadness alone does not make for a diagnosis of depression. Changes in sleep and appetite should be present as well as psychological symptoms including hopelessness and guilt. Bombardier et al. [2] found somatic symptoms including changes in sleep, psychomotor activity, and appetite along with poor energy to be as predictive as psychological symptoms in diagnosing depression. Evaluating plans and efforts to reach The article by Dryden et al. [1] on depression following spinal cord injury (SCI) identifi es risk factors as well as the frequency of depression associated with traumatic SCI. The authors accessed the computerized hospital records of nearly 100% of the residents of a Canadian province for 4 to 6 years following a 2-year index period. Fully one third of those with SCI received a subsequent diagnosis of depression. This high percentage may actually be an underestimation given the universal underdiagnosis of depression. Thus, about half of all persons hospitalized for traumatic SCI may benefi t from treatment for depression. Clinicians need to have a high index of suspicion for diagnosing depression in this population and a low threshold for initiating treatment. Untreated or inadequately treated depression is one of the most signifi cant contributors of reduced quality of life. Comparisons with numerous medical disorders have found depression to have a more profound negative effect on day-to-day functioning than most medical conditions. As Dryden et al. [1] make very clear, comorbid depression has a severe negative impact on post-SCI recovery ‘including longer lengths of stay for inpatient rehabilitation, less independence following discharge, poor compliance with self-care needs, higher medical expenses, and increased risk of suicide’. These only add to the abject misery, which accompanies depression. Published online: June 8, 2005

A case of the corpus callosum and alien hand syndrome from a discrete paracallosal lesion

Here we present a patient with an isolated paracallosal brain lesion who exhibited behavioral changes associated with the corpus callosum syndrome (CCS) including features of the alien hand syndrome (AHS). The CCS is also known as the split-brain syndrome, the syndrome of hemisphere disconnection, the syndrome of brain bisection and the syndrome of the cerebral commissures. Because most reported cases of CCS were caused by tumors which extended beyond the corpus callosum (CC) and did not always induce a complete disconnection, there was much controversy about the role of the CC and the existence of a specific CCS. Aside from surgically based cases, the full complement of the CCS is infrequently clinically encountered. The patient described has a classic CCS from natural causes. This case report is unique in exhibiting a complete CCS with AHS secondary to an ischemic event affecting the left pericallosal region. To our knowledge this is the first case report of such a combination.

Thirty-four hour dexamethasone suppression test in depression

The utility of extending the dexamethasone suppression test past its usual 24 hr period to include a cortisol determination at 34 hr was investigated in 18 depressed patients. Conventional suppressors and non-suppressors differed significantly on their 34 hr cortisol values. However, this difference was small. Furthermore, 34 hr values generally returned close to baseline values, so that the 34 hr DST cannot now be recommended in the assessment of depressed patients without further study.

Dextroamphetamine and dexamethasone suppression test prediction of desipramine response

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Neuroleptic radioreceptor activity and clinical outcome in schizophrenia.

The relationship between serum haloperidol concentration and clinical response was examined in 27 schizophrenic inpatients between the ages of 18 and 56 years. All patients were treated with haloperidol, 20 mg/day for the first 2 weeks. Dosage adjustment after 2 weeks of treatment was made in seven subjects based on poor clinical response or side effects. Haloperidol activity was determined by the radioreceptor assay for neuroleptics on weeks 2 and 4 serum samples. The results indicated that higher radioreceptor activity levels, particularly above 22 ng/ml, were associated with poorer clinical response. The data suggest that radioreceptor activity levels are not at a steady state after 2 weeks drug treatment. Additionally, problems secondary to low sensitivity of the radioreceptor assay may limit its utility at low serum concentrations.