Severe HS can be life-threatening, and nearly 30% of survivors suffering from permanent neurological sequelae. The damage of the HS to the central nervous system is caused by a variety of factors. The heat itself is directly toxic to brain cells (such as Purkinje cells of the cerebellum)[6]. Excessive secretion of cytokines such as interleukin-1 can disrupt the blood-brain barrier, which in turn leads to vasogenic edema[7]. It has been reported that lesions in a HS patient show high intensity on DWI and hypointensity on ADC may indicate cell-derived edema rather than vasogenic edema[8]. DIC can cause intracerebral hemorrhage, and microthrombus derived from DIC can cause small vessel ischemic injury. Incomplete circulatory function can lead to cerebral ischemia and hypoxia injury. Metabolic disorders can cause myelin to dissolve[9]. In addition, recent studies have shown that excitotoxic injury may also be involved in the pathogenesis of heat stroke. Li J and his coworkers found that the NAA/Cr value was low on magnetic resonance spectroscopy imaging of HS patients[10].
For many years, only a few scattered cases have been reported in the literature to document the imaging findings of the central nervous system. Brain lesions caused by HS are usually symmetrical in imaging examination. Summarizing the MRI reported in the literature, the lesions are mainly distributed in the cerebellum, thalamus, basal ganglia, cerebral cortex, brainstem, hippocampus, subcortical white matter, external capsule and splenium. The lesions of the cerebellum are mainly concentrated in cerebellar cortex, superior cerebellar peduncle, vermis of cerebellum, corpora dentatum. Besides, the caudate nucleus of basal ganglia are high-incidence areas [6, 7, 9, 11-18]. However, our case presents symmetrical lesions of both sides of the posterior limb of internal capsule, putamen, external capsule and insula lobe, and subcortical white matter, which has not been reported before. Due to the selective vulnerability of cerebellar neurons and Purkinje cells to thermal damage[14, 19], HS is prone to damage the cerebellum. Many HS patients show cerebellar symptoms such as ataxia[20]. However, no abnormal signals of the cerebellum were found on the MRI of our patient. Although some studies have found cerebellar atrophy delays on radiographic images[21].
It is reported in the literature that brain damage caused by HS is hyperintense lesions in the combination of the following imaging sequences: T2WI and FLAIR[9, 11], DWI and FLAIR[12], T1WI and T2WI. Sometimes these anomalous signals are limited to DWI[13]. However, the lesions in our case showed high and low mixed signals in the above sequences. Sometimes lesions can be enhanced on contrast-enhanced examination. It has been reported that cerebral lesions of HS patitent show punctiform hemorrhage on SWI[22].
Shock is one of the numerous risk factors for CVT[23]. Dentali F et al. reported that the sensitivity of D-dimer in CVT was 94%[24]. The deep venous system consists of straight sinus, vein of Galen and internal cerebral veins. MRI of DCVT can often observe bilateral thalamic lesions involving the basal ganglia[25]. At the time of admission, the patient suffered a shock and his D-dimer level was increased. Due to bilateral basal ganglia lesions, we prescribed MRV examination and found abnormalities. It is rare in previous literatures to mention MRV changes in patients with HS, so this case deserves to be reported. Interestingly, the patient's lesions were mainly located in the bilateral basal ganglia without thalamic, which is different from the common lesions of DCVT. Two previous studies have shown that low molecular weight heparin is more suitable for the treatment of CVT than unfractionated heparin[26, 27]. In general, CVT can achieve a good prognosis after treatment. In a study by Arauz A et al., approximately 90% of patients with obstructed cerebral veins were recanalized[28]. After the patient was treated with low molecular weight heparin, the second MRV showed recanalization of the straight sinus and vein of Galen.
The mechanism of brain damage caused by HS is complex and diverse, and its cerebral imaging changes are various. We report a patient with high and low mixed signals of bilateral posterior limb of internal capsule,putamen,external capsule and insula, and subcortical white matter on MRI, and his MRV showed the formation of DCVT. After treatment, his deep venous system was recanalized. We believe that when the cerebral MRI findings of HS patient need to be identified, MRV and other related tests should be performed, and timely treatment can improve the prognosis.