Hyperthermia after discontinuance of levodopa and bromocriptine therapy

L, Figà-Talamanca; Gualandi, Carla; Meo, Luciana Di; Battista, Giancarlo Di; Neri, Giuseppe; Russo, Francesca

doi:10.1212/wnl.35.2.258

Cited by 73 publications

(16 citation statements)

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“…Neuronal circuits involved in thermoregulatory mech anisms have also been identified in the mesencephalon, pons, medulla oblongata and spinal cord as well as in the basal gan glia, limbic system and cerebral cortex [6]. In the present study, the deficit of the sweating regulation mechanism is probably due to a damage of these central ANS tracts.…”

Section: Discussionsupporting

confidence: 61%

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Sweating Dysfunction in Parkinson’s Disease

Turkka

Myllylä²

1987

Eur Neurol

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Sweating was measured with an evaporimeter in 5 different positions on both sides of the body in 23 patients with idiopathic Parkinson’s disease and in 11 age-matched control subjects before and after a heating stimulus. Perspiration was increased significantly both before and after the heating provocation in the upper part of the body (the forehead, chest and forearm) of Parkinson patients in comparison with the control subjects (p < 0.05). The increase of perspiration correlated significantly (p < 0.05) with the severity of Parkinson’s disease as estimated by the Webster scale. The results indicate wide and clear autonomic nervous system dysfunction in Parkinson’s disease.

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Section: Discussionsupporting

confidence: 61%

“…The disturbed sweating is a common but scantily investigated feature in PD patients [1,3,6,7], although it is one of the most prominent aspects of the ANS disorders. The patients usually complain of diffuse exces sive sweating, commonly on the upper part of the body, especially on the face bilaterally.…”

Section: Introductionmentioning

confidence: 99%

Sweating Dysfunction in Parkinson’s Disease

Turkka

Myllylä²

1987

Eur Neurol

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“…The role of dopamine in this context brings back the concept of the acute autonomic overlap syndromes, particularly the aetiology of NMS (which is entirely neurotransmitter driven) and PHS (combining dopaminergic neuron loss, dopamine blockade and overresponsiveness to afferent stimuli) [65][66][67]. There are multiple case reports suggestive of post-TBI NMS [13,43,[68][69][70].…”

Section: Observations Regarding Neurotransmitter Effectsmentioning

confidence: 99%

A Critical Review of the Pathophysiology of Dysautonomia Following Traumatic Brain Injury

et al. 2007

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The management of Dysautonomia following severe traumatic brain injury (TBI) remains problematic, primarily due to an inadequate understanding of the pathophysiology of the condition. While the original theories inferred an epileptogenic source, there is greater support for disconnection theories in the literature. Disconnection theories suggest that Dysautonomia follows the release of one or more excitatory centres from higher centre control. Conventional disconnection theories suggest excitatory centre/s located in the upper brainstem and diencephalon drive paroxysms. Another disconnection theory, the Excitatory:Inhibitory Ratio (EIR) Model, suggests the causative brainstem/diencephalic centres are inhibitory in nature, with damage releasing excitatory spinal cord processes. Review of the available data suggests that Dysautonomia follows structural and/or functional (for example raised intracerebral pressure or neurotransmitter blockade) abnormalities, with the tendency to develop Dysautonomic paroxysms being more closely associated with mesencephalic rather than diencephalic damage. Many reports suggest that paroxysmal episodes can be triggered by environmental events and minimised by various but predictable neurotransmitter effects. This article presents a critical review of the competing theories against the available observational, clinical and neurotransmitter evidence. Following this process, it is suggested that the EIR Model more readily explains pathophysiological and treatment data compared to conventional disconnection models. In particular, the EIR Model provides an explanatory model that encompasses other acute autonomic emergency syndromes, accommodates 'triggering' of paroxysms and provides a rationale for all known medication effects.

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“…These symptoms include varying degrees of tremor; muscle rigidity; autonomic instability (manifested by tachycardia, hypertension, and diaphoresis); delirium; elevation of serum CPK; and in some cases, fever. Similar symptoms have been noted after the rapid cessation of levodopa or bromocriptine [16][17][18]. The severity of symptoms and the presence of fever are important distinctions in classifying patients along a spectrum of amantadine withdrawal from worsening tremor to neuroleptic malignant syndrome (NMS).…”

Section: Has a Syndrome Of Amantadine Withdrawal Been Described?mentioning

confidence: 81%

Case files of the Program in Medical Toxicology at Brown University: Amantadine withdrawal and the neuroleptic malignant syndrome

Brantley¹,

Cohn²,

Babu³

2009

J. Med. Toxicol.

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A sixty-one-year old woman with a history of depression and idiopathic dystonia presented to the emergency department (ED) with fever, nausea, muscle rigidity, and redness in her extremities. The patient had seen various specialists for her dystonia during the preceding year and had tried multiple medication regimens, including benztropine and tizanidine. The patient described her home medications as tizanidine 2 mg three times daily, diazepam 2.5 mg daily, escitalopram 100 mg daily, rosuvastatin 10 mg daily and bupropion 300 mg nightly.At ED presentation her vital signs were: temperature 37.5°C (99.5F), blood pressure 157/76 mmHg, heart rate 105 beats per minute, respirations 24 per minute, and oxygen saturation of 100% on room air. Her physical examination was significant for diaphoresis, tachycardia, diffuse flushing, tremors in her upper and lower extremities, muscle rigidity, and hyperreflexia in the upper and lower extremities. The tremors were low amplitude and worse with intention, while the rigidity had cogwheeling features and was more notable in her lower extremities. Initial laboratory evaluation was significant for a creatine phosphokinase (CPK) of 1146 IU/L. Her electrocardiogram showed sinus tachycardia with normal QRS and QT intervals, and no evidence of acute ischemia.Two months earlier, the patient's neurologist had started her on amantadine 100 mg twice daily for dystonia. Three days prior to ED presentation, the patient abruptly stopped taking her amantadine on the advice of a pharmacist, secondary to bilateral lowerextremity edema. The following day, the patient presented to her primary care physician complaining of nausea, tremors, and diffuse flushing. The physician treated her for an allergic reaction with oral steroids and diphenhydramine. The patient's symptoms worsened over the next day with increasing tremors and rigidity, low-grade fever, nausea, and flushing, which prompted her presentation to the ED.

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Hyperthermia after discontinuance of levodopa and bromocriptine therapy

Cited by 73 publications

References 0 publications

Sweating Dysfunction in Parkinson’s Disease

Sweating Dysfunction in Parkinson’s Disease

A Critical Review of the Pathophysiology of Dysautonomia Following Traumatic Brain Injury

Case files of the Program in Medical Toxicology at Brown University: Amantadine withdrawal and the neuroleptic malignant syndrome

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