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Table of Contents    
Year : 2017  |  Volume : 65  |  Issue : 5  |  Page : 1146-1148

Magnetic resonance imaging findings in heat stroke-related encephalopathy

1 Consultant Radiologist, Yashoda Hospital, Malakpet, Telangana, India
2 Consultant Physician, Yashoda Hospital, Malakpet, Telangana, India
3 Department of Radiology, Yashoda Hospital, Malakpet, Telangana, India
4 Consultant Neurologist, Yashoda Hospital, Malakpet, Telangana, India

Date of Web Publication6-Sep-2017

Correspondence Address:
Ravi K Jakkani
Consultant Radiologist, Yashoda Hospital, Malakpet, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/neuroindia.NI_740_16

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How to cite this article:
Jakkani RK, Agarwal VK, Anasuri S, Vankayalapati S, Koduri R, Satyanarayan S. Magnetic resonance imaging findings in heat stroke-related encephalopathy. Neurol India 2017;65:1146-8

How to cite this URL:
Jakkani RK, Agarwal VK, Anasuri S, Vankayalapati S, Koduri R, Satyanarayan S. Magnetic resonance imaging findings in heat stroke-related encephalopathy. Neurol India [serial online] 2017 [cited 2022 Jan 28];65:1146-8. Available from: https://www.neurologyindia.com/text.asp?2017/65/5/1146/214082


A 44-year old female patient was brought to the emergency department of our hospital in an unconscious state. The patient had a history of high grade fever associated with headache, generalized weakness, and altered sensorium since a week with one episode of seizure. She was admitted in another hospital with a high temperature of 107°F and was referred to our centre as she was not responding to the treatment being administered and had a worsening of her neurological status. There was a history of excessive exposure to external heat for a few days prior to the onset of her symptoms. Physical examination showed fever with a temperature of 104°F and features of dehydration. Neurological examination showed a stuporous state with altered sensorium with the Glasgow coma scale of E1V1M1, with normal pupillary reaction to light and normal deep tendon reflexes. Respiratory, cardiovascular, and abdominal examinations were within normal limits. Laboratory tests showed an elevated total leucocyte count of 14000/cmm, with elevated creatine phosphokinase (CPK) levels of 1600 U/L, dyselectrolytemia with reduced serum sodium levels of 121mEq/L, altered renal parameters with an elevated serum creatinine of 3mg/dl, and deranged liver function tests with elevated liver enzymes [serum glutamic oxaloacetic transaminase (SGOT) being 656U/L and serum glutamic pyruvate transaminase (SGPT) being 211U/l]. Infective markers were negative for malarial parasites plasmodium vivax and falciparum, typhoid (widal test), scrub typhus, and viruses. After the clinical examination and laboratory tests, the provisional diagnostic possibilities included heat stroke with multi-organ failure or meningoencephalitis with septic shock.[1] The patient was further referred for an magnetic resonance imaging (MRI) of the brain with contrast, in view of her altered sensorium. MRI of the brain revealed symmetrical areas of diffusion restriction on diffusion weighted imaging (DWI) with low apparent diffusion coefficient (ADC) values of up to 85% seen in bilateral cerebellar hemispheres, caudate nuclei, thalami, and subcortical white matter [Figure 1], [Figure 2], [Figure 3]. No appreciable signal changes were noted in the brain parenchyma in other sequences. There was neither evidence of bleed nor of abnormal enhancement. Based on the clinical presentation and MRI imaging findings, we suggested the presence of brain parenchymal changes secondary to heat stroke, with the possibility of meningoencephalitis being less likely.[1] A lumbar puncture was performed to exclude the remote chance of development of meningoencephalitis, which showed a normal cerebrospinal fluid (CSF) cell count with elevation in sugar (the level being 121mg/dl) and normal protein and chloride levels. Based on the clinical and laboratory parameters as well as the CSF picture in conjunction with MRI findings, a final diagnosis of encephalopathy secondary to heat stroke was made.
Figure 1: (a-d) Axial and sagittal diffusion weighted images of brain demonstrate symmetric diffusion restriction in bilateral cerebellar hemispheres (white open arrows)

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Figure 2: (a and b) Axial diffusion weighted images of brain demonstrate diffusion restriction in bilateral thalami and caudate nuclei (white open arrows) and subtle areas of diffusion restriction in sub cortical white matter (black open arrows)

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Figure 3: (a-d) Symmetrical areas of diffusion restriction in bilateral cerebellar hemispheres with low apparent diffusion coefficient values

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Heat stroke is characterized by an elevated core body temperature over 40°C with failure of the thermoregulatory mechanism.[2] The immediate complications of severe heat stroke include shock, acute respiratory distress syndrome, acid-base or electrolyte disturbances, disseminated intravascular coagulation, and rhabdomyolysis.[2] The central nervous system is very sensitive to hyperthermia, causing neurological complications due to involvement of the cortex, cerebellum, basal ganglia, anterior horn cells of the spinal cord, and peripheral nerves.[3] Initially, during hyperthermia, peripheral vasodilatation predominates to facilitate heat loss through the skin. To avoid a functional hypovolemia, a compensatory vasoconstriction of the splanchnic and renal vasculature occurs, often causing the symptoms of nausea, vomiting, and diarrhoea. If the heat stress continues, the compensatory vasoconstriction will eventually fail, further increasing the body temperature. Concurrently, cerebrovascular congestion and cerebral edema occur with the hyperthermia, causing an increase in intracranial pressure. Combined with a failure of splanchnic vasoconstriction and decreased mean arterial pressure, the cerebral blood flow falls.[4],[5] This results in cerebral ischemia. An aberration in coagulation is caused by a decrease in protein C, protein S, and antithrombin III, as well as alterations in vascular endothelium, creating a pattern resembling sepsis and disseminated intravascular coagulation.[4] This can cause hemorrhage within the brain, also resulting in neurologic dysfunction.[5] All of these physiologic processes occur concurrently, causing the common outcome of neuronal dysfunction.

It is of interest to note that in the cerebellum, thermal injury itself may cause destruction of the Purkinje cells. Increased production of heat shock proteins within the rabbit cerebellum during hyperthermia indicate that the Purkinje cells may require the activation of additional reparative mechanisms following a thermal injury. Therefore, in addition to being susceptible to hypoxic-ischemic injury, there is evidence that Purkinje cells are also susceptible to direct thermal injury.[6]

Though there have been several studies and postulation on the mechanism of heat stroke, there is not much information on the typical location of the brain injury that occurs due to the heat stroke. Postmortem studies dating back from 1916 to 1956 showed damage to the cerebellum, with additional findings in the cortex and brain stem.[7],[8] Bazille et al., in 2005 showed cerebellar atrophy as a common finding in a series of three patients in whom postmortem examination was conducted.[9] Previous radiologic studies have shown delayed cerebellar atrophy as a typical finding in line with this recent postmortem study. Many patients with heat stroke often present with cerebellar symptoms such as ataxia.[7],[10],[11]

Diffuse cortical abnormalities have also been described in patients with heat stroke. A case report from 1996 of a child suffering from heat stroke revealed diffuse cerebral edema with eventual cortical laminar necrosis in the vascular watershed zones, suggestive of an ischemic component to the mechanism of heat damage.[12] A few scattered case reports have revealed absence of cortical involvement with heat stroke. In 1995, Biary et al., published a report in which a brain MRI performed 2 weeks after the heat stroke revealed increased T2 signal within the left caudate nucleus, as well as bilateral subcortical and periventricular white matter followed by diffuse cerebellar atrophy after 6 months.[13]

Another case report of a patient with heat stroke revealed bilateral external capsule, bilateral putamen, and bilateral cerebellar involvement with associated presence of blood products on T2- and T1-weighted images and some enhancement on gadolinium images. The authors suggested small-vessel ischemia as being the responsible etiology for the findings, given that this type of presentation is often seen in subacute infarction. They also proposed that the cerebellar findings were MRI precursors for delayed atrophy, that had been subsequently seen in the previously reported cases.[14]

A publication in 2007 showed a case of patchy junctional zone involvement in bilateral hippocampi, as well as bilateral cerebellar abnormalities, as visualised on T2/FLAIR MRI images in a pediatric patient who suffered from heat stroke.[15] Though the radiological and autopy findings vary in the few reported cases, the cerebellum seems to be especially vulnerable to heat-induced injury. This is somewhat expected given the known sensitivity of the Purkinje cells to direct heat damage.

Cerebellar syndromes have also been reported after stroke. A case published by Fushimi et al., showed diffusion restriction in dentate nuclei, bilateral superior cerebral peduncles and central tegmentum of the midbrain, thus, following the course of the cerebellar efferent pathway.[16]

Liet al., studied the neurological damage that occurred due to heat stroke by diffusion tensor imaging. They showed the presence of a decrease of functional anisotropy values in these patients despite a normal appearing cerebellum.[17] They also studied the MR spectroscopy changes in patients suffering from heat stroke. These patients showed a low N-acetyl aspartate (NAA) peak with significant difference in the NAA/creatine ratio of the cerebellum between the patients and control volunteers, suggesting the concurrent presence of cerebral hypoxia and ischemia.[18] These findings may aid in evaluating the prognosis.

Our case who had suffered from heat stroke demonstrated diffusion restriction in bilateral cerebellar hemispheres, caudate lobe, thalami, and subcortical white matter due to cytotoxic edema. The present findings may be due to a combination of direct thermal injury and hypoxic ischemic injury. The differential diagnosis of cerebral cortical lesions in this case might include other abnormal neurological conditions such as postictal encephalopathy, encephalitis, or posterior reversible encephalopathy;[19],[20] however, there was no other clinical or laboratory evidence suggestive of the presence of any of these entities. The involvement of subcortical white matter corresponded to vascular junctional zones, which are more susceptible to ischemia, as described by Akaboshis et al.[12]

Our case also demonstrated significant involvement of bilateral cerebellar hemispheres, as mentioned in various case reports, suggesting the cerebellum to be the area most susceptible to heat injury. A postmortem report by Bazille et al.,[9] in patients of heat stroke showed that the predominant neuropathological change was an almost total loss of Purkinje cells, with additional involvement of the dentate nuclei of the cerebellum and the centromedian nuclei of the thalamus. An increased expression of heat shock protein 70 (HSP70), a chaperone protein having the ability to survive lethal stress, has been found near the remaining Purkinje cells and the adjacent Bergmann glia.[9]

In summary, heat stroke may produce multiple brain lesions such as ischemia, infarction, inflammation, and haemorrhage, with remarkably symmetric lesions being detectable in the cerebellum. Though MRI scan in not a requisite for the diagnosis of heat stroke, sometimes it is performed to exclude edema, hemorrhage, and other possible sequel of hyperthermia. DWI usually show abnormalities more conspicuously than T2 and fluid-attenuated inversion recovery images. The MRI findings observed following a heat stroke change over time; even if no abnormalities are apparent at the onset of heat stroke, the DWI findings obtained a few days after the heat-induced injury may provide some prognostic information.

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Conflicts of interest

There are no conflicts of interest.

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Fushimi Y, Taki H, Kawai H, Togashi K. Abnormal hyperintensity in cerebellar efferent pathways on diffusion-weighted imaging in a patient with heat stroke. Clin Radiol 2012;67:389-92.  Back to cited text no. 16
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