Adult aqueduct stenosis and diencephalic epilepsy

Bhigjee, Ahmed Iqbal; Ames, Frances R.

doi:10.1016/0022-510x(85)90038-3

Cited by 18 publications

(17 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These include spontaneous subarachnoid or intracerebral bleeds [8,19,37,38], pressure from tumours [3,6,8,9,[39][40][41], intra-aqueductal abscess [14], hydrocephalus [8,38,42] (occasionally in survivors of severe TBI) [12,43] and from cerebral hypoxia in the absence of other trauma [9,10,21,25,33,44,45]. Similar short-lived ANS changes are also seen in electroconvulsive therapy [46].…”

Section: Disconnection Theories and Observational Datamentioning

confidence: 78%

“…All Dysautonomic subjects in Strich's case series [33] exhibited spastic quadriparesis antemortem and at autopsy showed severe DAI, thalamic and brainstem damage with normal looking hypothalami. Bhigjee et al reported a case with an intra-aqueductal abscess with normal cortical and sub-cortical structures other than reduced periventricular white matter [14]. Penfield's original case report revealed a third ventricle cholesteotoma and a normal hypothalamus at post-mortem [6].…”

Section: Disconnection Theories and Observational Datamentioning

confidence: 97%

“…While seizure activity was first put forward to explain the syndrome [6], a subsequent review of the case suggested that some paroxysms were related to acutely increased intracerebral pressure (ICP) [7]. Furthermore, multiple attempts to either identify or treat epilepsy in Dysautonomic patients have produced negative results [8][9][10][11][12][13][14][15]. This is not to say that epilepsy cannot alter ANS function.…”

Section: Introductionmentioning

confidence: 93%

See 2 more Smart Citations

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

et al. 2007

View full text Add to dashboard Cite

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.

show abstract

Section: Disconnection Theories and Observational Datamentioning

confidence: 78%

Section: Disconnection Theories and Observational Datamentioning

confidence: 97%

Section: Introductionmentioning

confidence: 93%

See 1 more Smart Citation

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

et al. 2007

View full text Add to dashboard Cite

show abstract

“…In the latter report it was suggested that autonomic abnormalities represent epileptiform activities in some instances [2]. Other authors have considered paroxysmal autonomic abnormalities to be 'diencephalic seizures' or 'diencephalic epilepsy' [2,4,5]. Only 1 case of episodic hyperhidrosis without changes of thermoregulation or altered consciousness has been reported.…”

mentioning

confidence: 95%

Episodic Hyperhidrosis after a Journey to Southeast Asia

et al. 2000

View full text Add to dashboard Cite

“…Initially, because of the abnormal nature of related syndromes, epileptic discharges were considered as the mechanism of PSH [13]. Some people even used the term epilepsy or seizure to describe the syndrome of PSH.…”

Section: Introductionmentioning

confidence: 99%

Treatment Progress of Paroxysmal Sympathetic Hyperactivity after Acquired Brain Injury

Feng

Zheng

Fang³

2015

Pediatr Neurosurg

View full text Add to dashboard Cite

Paroxysmal sympathetic hyperactivity (PSH) is a common complication of various acquired brain injuries such as traumatic brain injury, subarachnoid hemorrhage, anoxic brain injury, intracerebral hemorrhage, and others. It is manifested by tachycardia, hypertension, tachypnea, diaphoresis, and dystonic posturing. The development of PSH can prolong hospitalization and lead to secondary brain injury and even death. Despite the awareness of the serious clinical impact, there is no consensus on diagnostic criteria. Thus, misdiagnosis and delayed recognition is very common. Most of the current treatment programs come from case reports and small case series; there are very few large-scale randomized controlled trials. Generally accepted medications are opioids, β-blockers and gabapentin (usually used in combination). However, the efficacy of these drugs has not been systematically assessed. The purpose of this review is to determine the treatment strategies and drugs commonly used for PSH at the overall level.

show abstract

Adult aqueduct stenosis and diencephalic epilepsy

Cited by 18 publications

References 16 publications

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

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

Episodic Hyperhidrosis after a Journey to Southeast Asia

Treatment Progress of Paroxysmal Sympathetic Hyperactivity after Acquired Brain Injury

Contact Info

Product

Resources

About