The featured paper today is a case study (freely available here) and is titled ‘Neurogenic T-wave inversion in pure left insular stroke associated with hyperhomocysteinaemia’. This is a letter to the Journal of Neurology, Neurosurgery and Psychiatry by J Mandrioli, A Zini, M Cavazzuti and P Panzetti. I’ve selected this case study to continue the theme of looking at the Insular Cortex although I think case studies are more useful for indicating possible directions for research.
The authors describe a 68-year old lady who presented with right sided ataxic hemiparesis, facial and hypoglossal nerve palsy as well as dysarthria. My first thought here was about a possible brainstem infarct. The hypoglossal and facial nerve nuclei are relatively closely related in the brainstem. Hemiparesis occurs when there is interruption of the corticospinal tract but these cross-over at the level of medulla and so we can also make some further inferences about the level of the lesion in this case (i.e. brainstem versus medulla). Dysarthria can be accounted for by lesions affecting the facial and hypoglossal motor nuclei amongst others. At this stage the lady presented with a left anterior hemiblock which may indicate other cardiac pathology although a later cardiac work-up was otherwise unremarkable (other than the T-wave inversion which developed later). What is interesting about this possibility of brainstem involvement is that the brainstem cardiovascular centre is thought to lie very close to the dorsal root nucleus of the vagus nerve which is located very close to both the hypoglossal and facial motor nuclei. What seems to count against this is the MRI and CT scan findings which show that there was only involvement of the Insular cortex. However MRI and CT scans don’t always pick up brainstem lesions. Thus another study looked at clinically definite brainstem ischaemic stroke and found that MRI detected this in 79% of cases and CT in 33% (the article is freely available here).
The lady’s symptoms resolve and she is discharged, only to be readmitted with similar symptoms. This time however she has in addition ‘non-fluent aphasia with phonemic paraphasia, anomia’. These symptoms are suggestive of involvement of the frontal and temporal lobes and so the picture is a quite curious one. On investigation the lady is found to have elevated homocysteine levels which have been associated with ischaemic events and were thought to be responsible for the lady’s presentation. The T-wave inversion persisted (indeed the authors refer to this as ‘persistent neurogenic T wave alteration) and the authors suggest that this resulted from Insula involvement citing other pieces of relevant research.
I would prefer to draw three possible interpretations
1. Lesions to the Insula Cortex can result in T-wave inversion
2. The elevated homocysteine levels caused T-wave inversion directly. This is supported by a case 3 in a case series (freely available here) showing T-wave inversion and abnormalities in the apical wall movements on echocardiography together with hyperhomocystinaemia!
3. There was possible brainstem involvement which led to T-wave inversion. In this regards natural mechanical stimulation of the medulla in humans has been found to decrease T-wave amplitude (in a paper freely available here).
I’ve just included 2 assumptions here derived from this paper which could be useful in developing a model of the Insular Cortex
1. Brain lesions secondary to cerebrovascular events can produce cardiac arrythmias even in the absence of other cardiac pathology (The authors cite Oppenheimer S, 1990 to support this assertion).
2. The Insula Cortex is involved in cardiovascular control including heart rate (The authors cite Tokgozoglu SL et al, 1999 to support this assertion).
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