Affiliations: Cognitive Neurology Division, Department of Neurology,
University of South Florida, Tampa, FL 33612, USA. E-mail:
mhoffman@health.usf.edu
Abstract: 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.
