Pathophysiology of transient neurological deficit in patients with chronic subdural hematoma:A systematic review

Patients with chronic subdural hematoma (CSDH) can have transient neurological deficits deficit (TND) mimicking transient ischemic attacks. The prevalence of TNDs in CSDH varies between 1%–24%, depending on TND definition. Despite this high prevalence the pathophysiology of TND in CSDH is not clear in many cases. In this systematic review, we aim to unravel the responsible mechanism. Pubmed and Embase were searched for all articles concerning the pathophysiology of TND as a presenting symptom in patients with CSDH. There were no publication date restrictions for the articles in the search. Two reviewers independently selected studies for inclusion and subsequently extracted the necessary data. Out of 316 identified references, 15 met the inclusion criteria. Several articles mentioned multiple pathophysiological mechanisms. One of the proposed etiologies of TND was epileptic activity, stated by three articles. In contrast, three different studies stated that seizures are unlikely to cause TND. Five papers suggested that obstruction of blood flow, caused by the hematoma or subsequent swelling, might be the cause. Six articles made no definite statement on the responsible pathophysiological mechanism of TND. Different mechanisms have been proposed to be the cause of TNDs in patients with CSDH. Based on this review, the exact pathophysiology of TND remains unclear. We suggest that future studies on this topic should incorporate MRI of the brain (with diffusion-weighted imaging) and EEG, to provide better insight into TND pathophysiology. The knowledge resulting from future studies might contribute to better understanding of TND and optimal treatment in CSDH

Transient neurological deficit in patients with chronic subdural hematoma:a retrospective cohort analysis

RATIONALE: Symptoms of chronic subdural hematoma (CSDH) vary widely, including transient neurological deficit(s) (TND). The precise prevalence and the clinical aspects of TND are yet to be determined. Most TNDs are regarded and treated as symptomatic seizures, but the rationale for this decision is not always clear. METHODS: Patients with temporary symptoms were selected from a retrospective cohort of CSDH patients. We analyzed the association of TND characteristics with patients being classified as having a symptomatic seizure and with functional outcome using logistic regression analysis. RESULTS: Of the included 1307 CSDH patients, 113 (8.6%) had at least one episode of TND. Most common TNDs were aphasia/dysphasia, impaired awareness or clonic movements. Of these 113 patients, 50 (44%) were diagnosed with symptomatic seizure(s) by their treating physician. Impaired awareness, clonic movements and the presence of 'positive symptoms' showed the strongest association with the diagnosis symptomatic seizure (OR 36, 95% CI 7.8-163; OR 24, 95% CI 6.4-85; and OR 3.1, 95% CI 1.3-7.2). Aphasia/dysphasia lowered the chance of TND being classified as symptomatic seizure together with a longer TND duration (OR 0.2, 95% CI 0.1-0.6; and OR 0.91, 95% CI 0.84-0.99). Treatment with anti-epileptic drugs was related to unfavorable functional outcome (aOR 5.4, 95% CI 1.4-20.7). CONCLUSION: TND was not a rare phenomenon in our cohort of CSDH patients. A TND episode of 5 min, aphasia/dysphasia and/or absence of 'positive' symptoms are suggestive of a different TND pathophysiology than symptomatic seizures. Our results further suggest that treatment of TND in CSDH deserves careful consideration as management choices might influence patient outcome