Post-Sroke Mania: A Case Series in a Rural, Community Hospital

Department of Family Medicine, University of New England College of Osteopathic Medicine, USA

*Corresponding author: Dr. Mehl-Madrona, Associate Professor, Department of Family Medicine, Eastern Maine Medical Center, Acadia Hospital, Coyote Institute, University of New England College of Osteopathic Medicine, USA, Tel: 808-772-1099, E-mail: lewis.mehlmadrona@umaine.edu
J Geriatr Med Gerontol, JGMG-2-015, (Volume 2, Issue 2), Case Series; ISSN: 2469-5858
Received: May 02, 2016 | Accepted: September 10, 2016 | Published: September 12, 2016
Citation: Mehl-Madrona L (2016) Post-Sroke Mania: A Case Series in a Rural, Community Hospital. J Geriatr Med Gerontol 2:015. 10.23937/2469-5858/1510015
Copyright: © 2016 Mehl-Madrona L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background and purpose: Post-stroke mania is thought to be rare, and has been described after lesions in the territory of the left medial cerebral artery, biparietal cortex, and the left putamen.

Methods: Case-study methodology was used to identify similarities and difference among six cases of post-stroke mania in a rural, community hospital over 1 year.

Results: All patients had pre-existing moderate levels of small vessel occlusive disease and two had confirmed lacunar infarcts in the basal ganglia, while one had a small left sided fronto-parietal infarct consistent with the dysarthria-clumsy hand syndrome. Stroke was not initially recognized among these patients due to the absence of acute CT findings. Patients without pre-existing psychiatric diagnoses responded to low dose quetiapine. Two patients with pre-existing diagnoses of depression and anxiety, required higher doses.

Conclusions: Post-stroke mania may be under-appreciated due to the subtle neurological findings inherent to basal ganglia and/or lacunar infarcts in other locations. Acute CT is not reliable enough to confirm the diagnosis of stroke which may allow many of these cases to be missed.

Keywords

Post-stroke mania, Small vessel disease, Cerebrovascular disease

Introduction

Mania rarely occurs for the first time in late life [1]. A systematic review found only 74 reported cases of adult stroke patients with mania symptoms in the last 50 years, suggesting that mania is a rare consequence of stroke [2]. When it does occur, it often presents atypically with a mixture of manic, dysphoric, and cognitive symptoms and less euphoria than is seen in younger, more typical cases [3]. Increased cerebral vulnerability due to stroke or head trauma play a stronger role than life events in precipitating late-onset mania among the elderly [3,4]. The most relevant findings on imaging in late onset mania are silent cerebral infarctions and subcortical lesions [5]. Secondary mania has been documented in 17 to 43% of manic cases in the elderly and has been associated with a higher prevalence of cerebral organic disorders [6] especially cerebrovascular disease [7], dementia [8], space occupying lesions, infections, and head injuries. Post-stroke depression is the most common psychiatric disorder following stroke, but mania has been reported [9].

Materials and Methods

We reviewed 6 cases of mania in elderly patients followed cerebrovascular events from our geriatric medicine consultation service over the course of 1 year. We summarize the similarities and differences among these cases and with others reported in the literature using the case report methodology of Kratochwill and Levin [10].

Results

Case 1

Case 2

Case 3

A 76-year-old woman was admitted to the hospital after a second fall. Two months previously, she had fallen at home in Florida. Since the first fall, her behavior had been erratic. She gave a distant great-niece, whom she had never seen, $80,000 from the proceeds of the sale of her home. She bought a new Cadillac. She impetuously and impulsively moved back to Maine, where her brother and his wife lived. Just before her second fall, she was preparing to give her distant great-niece another$40,000; to give the Komen Breast Cancer Fund, $10,000; and to give our hospital's cancer center,$25,000. Her brother had learned of these pending transactions and had blocked them using his power of attorney two days before her second fall and admission.

On admission, she was agitated and angry. On arrival to her room, we met an angry woman who couldn't stop talking about her brother violating her rights and preventing her from using her money as she saw fit. She was grandiose and pressured. She was irritable. She had no idea how much money she had and was unable to do arithmetic. Her neurological exam was positive only for increased lateral nystagmus and difficulty balancing on one leg, in tandem, on heels, or on tiptoes. Her sternal nudge was positive. Neuropsychological testing with the RBANS and subtests of the Wcchsler Adult Intelligence Scale (WAIS) revealed minor neurocognitive disorder. Her MRI scan revealed moderate periventricular small vessel disease. A new (in the past two months), small lacunar infarct was noted in the area of the basal ganglia using FLAIR MRI. Minimal brain atrophy was present. Her past medical history was positive for coronary artery disease, hypertension, diabetes, and hypercholesterolemia. She had no prior diagnosis of bipolar disorder, but had treated for years for anxiety disorder, mostly with benzodiazepines. We agreed that she lacked capacity to manage her finances. The great-niece stopped visiting and would not return our telephone calls. We reported the situation to the Agency on Elder Abuse. Due to her high levels of agitation in the evening, we started quetiapine 25 mg PO bid. This was enough to eliminate her agitation and irritation. She stilled wished to give away her money and believed she had the right to do so, but was not having tantrums about her brother preventing her from doing so. She was discharged to an assisted living facility for further acute rehabilitation. The physician in acute rehabilitation stopped her quetiapine (reason undocumented) and her irritability and pressured speech returned. We were consulted again on an outpatient basis, recommended restarting the quetiapine, and eventually titrated it to a dose of 50 mg PO twice daily, which produced less sedation than 100 mg PO at bedtime. This dose kept her from being irritable, pressured, and demanding of her rights to give away her money. She continued to do well on this dose over the next 8 months.

Case 4

Through 6 are summarized in table 1. Evidence of clinical stroke existed in each of these cases on FLAIR MRI scans. In all three cases, mania came after a definitive neurological event. These six cases emerged from 262 inpatient geriatric consultations, which suggest a more common prevalence than previously appreciated.

Table 1: Summary of the time course of events of the six patients with post-stroke mania. View Table 1

Similarities: All six patients had moderately severe small vessel occlusive disease in the periventricular white matter. Four had or developed lacunar infarcts in the area of the basal ganglia. Two had temporal lobe infarcts. None of the patients had a previous diagnosis of bipolar disorder. Four presented with problems with gait and balance. Subtle neurological findings existed on physical examination, which were not appreciated by the ED physician or the admitting hospitalist. The possibility of stroke contributing to these patient's psychiatric symptoms was minimized or denied by their hospitalists in relation to the absence of acute findings on the CT scan. Fall was a common sentinel event that brought these patients to the Emergency Department. While two of the patients had pre-existing minor neurocognitive disorder, none had major neurocognitive disorder.

Differences: Two of the patients had a pre-existing psychiatric history (depression and anxiety diagnoses) and required higher doses of quetiapine to manage their mania than the others who had no pre-existing psychiatric history.

Discussion

Our findings suggest that post-stroke mania may be more common than the current literature would suggest. Over one year in a rural 192-bed hospital, we encountered six cases (almost 2% of our geriatric consultations), and no cases of new-onset geriatric mania without a preceding neurological event. The neurological antecedents appear to be under-appreciated due to contemporary reliance on CT scanning to diagnose stroke versus clinical examination. We also noticed a tendency on the part of the hospitalists to not carefully assess gait and balance. The neurological findings may be subtle and transient and represent basal ganglia and/or lacunar infarcts in other locations. Our 6 patients convincingly demonstrated mania occurring after small cerebrovascular events.

Cognitive impairment, dementia, personality change, psychosis, apathy and anxiety all occur after stroke [11]. Lesions in the cerebral hemisphere and limbic structures may produce symptoms suggestive of mania. Right-sided cerebrovascular lesions involving regions connected to the limbic cortex have been implicated in late-onset mania [12]. In addition, secondary mania in right-handed people with dominant left hemisphere involvement is increasingly being recognized [13]. Removal of inhibitory tracks from the pre-frontal cortex to the limbic brain and ventral striatum may unmask mania that was previously kept in check. More attention should be directed to the basal ganglia and to small vessel occlusive disease in explaining new onset, geriatric psychiatric syndromes, and especially the role of basal ganglia lesions in post-stroke mania. The existence and sequelae of cerebral small vessel disease is only now becoming appreciated [ref], especially because the neurological findings are often transient and it may require diffusion tensor imaging to find the lesions to fiber tracts, a technology that most hospitals do not have.

The likelihood of developing a stroke is greater among patients with bipolar disorder than controls, and the all-cause mortality rate is higher among patients with bipolar disorder than controls [14]. Compared with schizophrenia patients, those with bipolar disorder were 19% more likely to have diabetes, 44% more likely to have coronary artery disease, and 18% more likely to have dyslipidemia, after adjustment for other factors [15].

Pathological generosity, as existed in one of our patients, has been described following a left lenticulocapsular stroke with hypoperfusion of several anatomically intact cortical areas [16]. A 49-year-old man developed excessive and persistent generosity as he recovered from a left lenticulocapsular hematoma. His symptoms resembled an impulse control disorder. (99m) Tc-HMPAO SPECT demonstrated hypoperfusion, mostly in the ipsilateral striatum, dorsolateral, and orbit frontal cortex. This case study adds pathological generosity to the range of behavioral changes that may result from discrete unilateral lesions of the lenticular nucleus and nearby pathways.

In another case report of post-stroke mania, SPECT scan performed during the manic state demonstrated hypoperfusion in the right temporal and frontal regions due to right putaminal hemorrhage [17], the site of lesion for one of our patients. It also showed hyperperfusion in the inferior lateral prefrontal lobe, the temporal lobe, and the medial and lateral parts of the parietal lobe in the left hemisphere. A second SPECT scan performed during the euthymic state demonstrated moderate improvement in the hypoperfusion in the right fronto-temporal regions. The focal hyperperfusion in the anterior insular cortex, inferior lateral prefrontal lobes, and superior-middle temporal gyrus in the left hemisphere had vanished.

Treatment of mania with even small doses of antipsychotic medication resolved the symptoms. The differentiation between neurological and psychiatric causation may not affect treatment, but it matters to families and to the care they receive. At least in our region, patients with psychiatric diagnoses are less likely to be accepted by assisted living facilities and skilled nursing facilities and are stigmatized more than patients with neurological diagnoses. Families also appear to be more comfortable with neurological explanations than that of late-onset bipolar disorder. The other lessons from this case series is the importance of a careful neurological examination after a fall, especially an assessment of gait and balance, and the avoidance of over-reliance on imaging to rule out small strokes in the presence of significant, albeit transient neurological findings.

Disclosures

None.

References