Korean Journal of Cerebrovascular Surgery 2001;3(1):78-80.
Published online March 1, 2001.
A Case of Right Middle Cerebral Artery Infarction with Quadriparesis.
Lee, Jee Youn , Han, Si Ryung , Kim, Yeong In
Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea. srhan@cmc.cuk.ac.kr
Diaschisis is classically defined as a sudden inhibition of function, produced by an acute focal disturbance in a remote area which is anatomically connected through fiber tracts. Transhemispheric diaschisis can underlie some diffuse symptoms of acute supratentorial stroke such as agitation, confusion, and coma. We experienced a patient with right middle cerebral artery infarction, presenting a quadriparesis and hypoesthesia at sensory level. This case suggests the diaschisis exacerbate the initial focal deficit such as weakness and sensory loss.
Key Words: Transhemispheric diaschisis, Middle cerebral artery infarction

   Remote metabolic effects are widely explained as the depressed synaptic activity at sites distant from, but neurally connected with the damaged area.1)4) As such, they allow us to map the disruption in distributed networks as a result of focal infarction. Although they are often referred to as diaschisis,4) a variety of cellular degeneration form reversible hypofunction to evolving degeneration is concealed in them. Some of these effects may represent purely functional trans-synaptic derangement, and thus may participate in both the acute clinical expression of and the subsequent recovery from stroke, they have attracted considerable interest over the last 15 years.

Case Report

   A 40-year-old right-handed woman was admitted with paresthesia below T12 and left crural monoparesis for 10 days. She felt an electrical sensation on the plantar surface of left foot 10 days before admission. 7 days later, she complained of left crural monoparesis. She denied having hypertension, diabetes mellitus, ischemic heart disease, and any other neurological illness. On the day of examination she was alert and attentive. Her score was normal on minimental examination. Her eye movement was normal and facial expression was symmetric. Motor power of left lower extremity was proximally grade IV and distally grade II. Sensory examination showed hypesthesia below T10 level on right side and below T12 level on left side including sacral area against pain, temperature and vibration. Deep tendon reflex of left lower extremity was hyper-reactive and plantar response was extensor. Bilateral Chaddok signs were present. MRI of thoracic spine at admission showed normal. One day after admission, she complained of ascending paresthesia on trunk below T4 level. Neurologic examination revealed her sensory level ascended unto T4 dermatome and there were bilateral Hoffmann signs. On the 3rd hospital day, she appeared slightly apathetic and her verbal output was decreased. She showed quadriparesis with bilateral Babinski signs on the motor exam. There were high signal changes on right fronto-parietal lobe on Diffusion-weighted brain MRI, which suggest acute infarction in right MCA territory. The perfusion-weighted MRI showed decreased cerebral blood flow and cerebral blood volume on bilateral fronto-parietal lobes. But, time to peak (TTP) and mean transit time (MTT) was normal in the left frontal lobe, suggesting metabolic depression (Fig. 1). C-spine MRI showed normal findings. On 7th hospital day, she showed improved course in verbal output and right side weakness.


   Widely hypothesized as transcallosal in nature, the phenomenon of contralateral cerebral hypometabolism has attracted great interest due to its clinical symptoms. However, it has proved difficult to document in either humans or the animals in the acute stage. Quite unexpectedly, metabolism in the contralateral hemisphere appears to reach its lowest level several days after stroke onset.6) Stuies that used CBF to evaluate this phenomenon in acutely ill patients were limited by the dependence of parameters on extracerebral physiologic variables, such as PaCO2 or hematocrit. A study in anterior circulation ischemic stroke that controlled for most of the above-mentionedd confounding factors also revealed a significantly reduced contralateral CBF in the subacute sage, but this effect did not correlate with the subject's lethargy score.3) Recently, iglesias et al6) reported no correlation between the degree and time course of contralateral cerebral CMRO2 and either initial neurologic deficit or recovery therefrom, suggesting that the level of contralateral metabolism play little or no part in the clinical ezpression of acute stroke. Overall, therefore, the presently available data suggest that contralateral cerebral hypometabolism does not develop acutely after MCA territory stroke but may slowly creep in within the first week and recover partly thereafter, an effect presumably related to transcallosal fiber degeneration.7)8)10) This subacute nature of diaschisis explain the clinical course of progression from left lower extremity weakness to right lower extremity weakness with one week gap.
   Perfusion-weighted MRI, typically deals with blood volume and transit time. Diaschisis is defined as a matched decrease in CBF, CBV, and CMRO2, without alteration in TTP and OEF, indicating that the normal perfusion-metabolism coupling is preserved.2)5)9)
   In conclusion, diaschisis phenomenon underlies the variable clinical neurological manifestations of acute stroke that all far exceed the size of the infarct. Rehabilitaion, pharmacological, and biological interventions might be developed to induce this palsticity and enhance neurologic recovery.


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