Etiology of Frontal Network Syndromes in Isolated Subtentorial Stroke

Background: The neurobiology of the frontal network syndrome (FNS) that may occur with isolated subtentorial stroke is unknown. Aim: Evaluate for frontal network syndromes in young people post subtentorial stroke who have recovered neurologically and compare to a stroke lesion group least likely to manifest frontal network syndromes. Methods: Young people (18–49 years) with isolated cerebellar or brainstem subtentorial stroke (ST) that had recovered to independency (Rankin score ࣘ 2) with minimal or no residual neurological deficit (NIHSS ࣘ 4) with neurological recovery enabling resumption of former employment. Comparison was made to age and education matched young people with posterior circulation territory parieto occipital lobe infarcts (PO). Depression, anxiety, systemic disease, autoimmune disease, neurodegenerative disease and substance abuse were specific exclusions. A battery of frontal tests surveying the principal frontal network syndromes (apathy, disinhibition, executive dysfunction, emotional intelligence quotient) was used. Neurological deficit and long tract signs were measured by the NIH stroke score (NIHSS). Results: From the cognitive stroke registry of young stroke patients (n = 511), analysis for isolated subtentorial infarction yielded cerebellar infarcts (n = 43, 8.4%) and brainstem infarcts (n = 36, 7.0%). After exclusions, 16 patients (cerebellum, n = 10, pons, n = 6) were compared to 10 PO infarct patients controlled for mean age, gender and NIH stroke scores. Overall 11/16 (69%) patients in the ST and 5/10 (50%) in the PO group manifested one or more of the principal FNS syndromes. Mean T scores for apathy, disinhibition, executive function and emotional intelligence standard scores were significantly more impaired in the ST group, but not for WCST error percentage scores. Conclusions: The mismatch of scant neurological deficit manifested by low NIHSS but with FNS in the majority of isolated ST stroke and more so than with PO stroke, gives support for a state dependent or neurotransmitter perturbation. The clinical impact is that such syndromes may be amenable to neuropharmacological intervention.