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Archived Comments for: Cerebral infarction in diabetes: Clinical pattern, stroke subtypes, and predictors of in-hospital mortality

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  1. Lacunar infarction: the enigma of a non-ischemic stroke subtype

    Vinod Gupta, Dubai Police Medical Services, Dubai, United Arab Emirates

    21 May 2005

    Arboix and colleagues present an in-depth analysis of stroke subtype occurrences in diabetic and non-diabetic patient populations as indexed in the stroke registry of a tertiary care centre in Spain. [1] The general perception of lacunar stroke is as a variant of cerebral ischemia commonly associated with atherothrombotic stroke; the concurrence of both stroke types makes it difficult indeed to conceptualize a difference in the pathogeneses of these two main subtypes of (?ischemic) stroke. Nevertheless, a statistically significant higher incidence of lacunar infarction has been seen in diabetic patients as compared to non-diabetic patient population. [1]

    Certain key clinical observations stimulate lateral thinking about lacunar infarctions. (i) Occurrence of lacunar lesions in MRI scans, with or without atherothrombotic infarcts, is not necessarily or always associated with neuroanatomically consistent functional losses. (ii) A particular topographic distribution characterizes lacunar infarcts, [2] the basis of which remains uncertain. A crucial anatomic difference exists between deep lenticular arterioles embedded in brain tissue and more superficial cortical arterioles. In states of sudden profound cerebral hyperperfusion, lenticular arterioles with limited distensibility are likely to be more susceptible to rheological barotraumas and to undergo segmental arteriolar wall disorganization (lipohyalinosis or fibrinoid necrosis). [3] Such a pressure distortion of deeper arterioles is far more likely to be "around" rather than at the "end" of the abnormal segment, [3] as has also been speculated. [4] (iii) White matter lesions (WML) are found in hypertensive encephalopathy, puerperal eclampsia, migraine, and therapy with cyclosporine, interferon-α, and tacrolimus. [5] Also, a characteristic difference prevails in the distribution of posterior circulation territory cortical infarcts and deep WML in migraine patients. [5] Prolonged, diffuse hyperperfusion prevails in the cerebral cortex, thalamus and basal ganglia in migraine. [6] Vasogenic cerebral oedema resulting from intense but-self limited cerebral hyperperfusion probably underlies WML in hypertensive encephalopathy and migraine.[2] The peculiar anatomically embedded distribution of the lenticular arteries render them more susceptible to episodic profuse cerebral hyperperfusion in hypertensive encephalopathy or migraine, which influences relatively spare the more superficial cortical arteriolar network. [5] As has been underscored recently, the role of hypertension in the genesis of lacunar infarctions must not be undermined. [3] (iv) As the authors have outlined, diabetes is associated with small vessel arteriolopathy in the retina, kidney and brain. [1] In seeking a mechanism for cerebral arteriolar endothelial failure, [4] we must ask why prolonged diabetes mellitus cannot affect pressure-sensitive walls of the lenticular arterioles as it does the retinal arterioles. [3] (v) The perfusion of the periventricular region where WML or “lacunes” are predominantly seen is particularly and inversely susceptible to variations of the brain cerebrospinal fluid (CSF) pressure. Sudden lowering of CSF pressure can induce episodic lenticular arteriolar dilatation and vasogenic oedema. [3] These three putative mechanisms for lacunar strokes are independent of influences affecting the progress of atherothrombotic disease. (vi) A diffuse cerebral arteriolar pathological vascular anomaly, as suggested, [1,4] is unlikely to underlie lacunar infarcts. The suddenness of the lacunar infarct also questions the operation of a presumed gradual pathological process diffusely affecting cerebral arterioles. Unpredictable progression of lacunar stroke symptoms or asymptomatic or randomly progressive (both in site and time of occurrence) additional lacunar infarcts further militates against an orderly pathophysiological process. [3] Whereas ischemic strokes consequent to atherothrombotic disease also can develop suddenly, once a critical level of cerebral atherosclerosis has set in, ischemic stroke recurrences are generally more frequent, more predictable, and more disabling than lacunar infarcts. (vii) Extremely good prognosis of lacunar infarcts (0% in-hospital mortality) [1] also dramatically separates this entity from ischemic atherothrombotic lesions. (viii) Transient global amnesia probably represents a particular variant of lacunar infarction -- the outcome of a non-ischaemic breakdown of the blood-brain barrier at the level of the medial temporal region that occurs randomly in patients susceptible to episodic brain hyperperfusion. [7]

    It is, nevertheless, particularly difficult to break out of our mindset that is moulded on the pattern of the ischemic stroke model, particularly given the concurrence [4] of small cortical infarcts with the lacunar syndrome. [3]

    References

    1. Arboix A, Rivas A, Garcia-Eroles L, de Marcos L, Massons J, Oliveres M. Cerebral infarction in diabetes: clinical pattern, stroke subtypes, and predictors of in-hospital mortality. BMC Neurology 2005,5:9.

    2. Kiers L, Davis SM, Larkins R, Hopper J, Tress B, Rossiter SC, Carlin J, Ratnaike S: Stroke topography and outcome in relation to hyperglycaemia and diabetes. J Neurol Neurosurg Psychiatry 1992, 55:263-270.

    3. Gupta VK. Lacunar stroke: on the threshold of a paradigm shift? J Neurol Neurosurg Psychiatry (13 May 2005). Available at:

    http://jnnp.bmjjournals.com/cgi/eletters/76/5/617

    4. Wardlaw JM. What causes lacunar stroke? J Neurol Neurosurg Psychiatry 2005;76:617-619.

    5. Gupta VK. White matter hyperintensities: pearls and pitfalls in interpretation of MRI abnormalities. Stroke 2004, 35: 2756-7;published online November 4 2004,

    doi:10.1161/01.STR.0000147158.89251.5b.

    6. Kobari M, Meyer JS, Ichijo M, Imai A, Oravez WT. Hyperperfusion of cerebral cortex, thalamus and basal ganglia during spontaneously occurring migraine headaches. Headache 1989, 29:282-289.

    7. Gupta VK. Transient global amnesia: consequent to brain hypoperfusion or hyperperfusion? J Neurology Neurosurgery Psychiatry (16 May 2005). Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/4/509#515

    Competing interests

    None declared

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