Forensic Sci Med Pathol (2013) 9:260–264 DOI 10.1007/s12024-012-9339-9

IMAGES IN FORENSICS

Patterns of cerebral and cerebellar herniation Roger W. Byard

Accepted: 6 April 2012 / Published online: 29 April 2012 Ó Springer Science+Business Media, LLC 2012

Anatomically the brain is compartmentalized by rigid folds of dura such as the falx cerebri which the lies between the cerebral hemispheres, and the tentorium cerebelli that separates the inferior portions of the occipital lobes from the cerebellum. When intracranial pressure increases, brain tissue may be compressed resulting in characteristic flattening of gyri and protrusion of tissue from one compartment into another. This may be caused by a diffuse increase in brain volume from edema due to trauma, or by a focal space occupying lesion such as hemorrhage, tumor or abscess [1]. Intracranial pressure may rapidly increase following hemorrhage or trauma [2]. The resultant herniations may be subfalcine, transtentorial (uncal), tonsillar or transcalvarial (Fig. 1) and may compress blood vessels resulting in critical compromise of circulation with local areas of infarction. The following provides a description and illustration of the major forms of herniation that may be encountered in forensic practice, with a discussion of possible secondary effects. Although the underlying lesions in the reported cases did not necessarily cause sudden and/ or unexpected deaths, they have been selected as they clearly demonstrate characteristic features of typical herniations.

unilateral expansion of a hemisphere by a tumor, forces the cingulate gyrus under the falx cerebri to the opposite side [3]. The falx may also shift away from the midline when there is significant unilateral pressure [4]. Case 1 A 62-year-old woman with a left temporal lobe glioblastoma multiforme with compression of the left lateral ventricle. A coronal section of the brain revealed prominent subfalcine herniation of the cingulate gyrus (Fig. 2). Case 2 Subfalcine herniation viewed from above showing the position of the falx (Fig. 3). Case 3 A 58-year-old man with a right middle cerebral artery infarction. Dissection of the brain shows compression of the right lateral ventricle with herniation of the right cingulate gyrus beneath the falx (Fig. 4). Secondary effects of subfalcine herniation include compression of pericallosal branches of the anterior cerebral artery with infarction [1].

Transtentorial herniation

This occurs when unilateral pressure on a cerebral hemisphere from, for example, a subdural hematoma, or

This occurs when increases in supratentorial pressure force the medial part of the temporal lobe, the uncus, downwards through the opening of the tentorium cerebelli [3]. Rarely a space occupying lesion in the cerebellum, such as a tumor or posterior fossa hemorrhage, may cause upwards herniation through the tentortium [4].

R. W. Byard (&) Discipline of Anatomy and Pathology, The University of Adelaide, Level 3 Medical School North Building, Frome Road, 5005 Adelaide, SA, Australia e-mail: [email protected]

Case 4 Increased intracranial pressure causing marked bilateral uncal herniation with notching (more on the right side) (Fig. 5).

Subfalcine herniation

123

Forensic Sci Med Pathol (2013) 9:260–264

261

Case 5 A 76-year-old woman collapsed with a left intracerebral hemorrhage. At autopsy marked notching of the left uncus and parahippocampal gyrus was noted (Fig. 6). Secondary effects of uncal herniation include compression of the third cranial nerve and the contralateral cerebral peduncle. If these secondary effects have occurred there may be a history of a fixed dilated pupil with abnormal ocular movement on the side of the lesion, or of paradoxical ipsilateral hemiparesis [1]. Grooving of the peduncle is referred to as Kernohan’s notch [5]. Pressure on branches of the posterior cerebral artery may result in infarcts of the posterior inferior temporal lobe and the medial occipital lobe that are most often hemorrhagic. As this may involve the optic area of the cortex this may have manifested clinically as either homonymous hemianopia, or complete cortical blindness with bilateral herniation [4]. Another effect of acute and asymmetric herniation through the tentorium is the production of linear or flameshaped hemorrhages in the midbrain and pons [4]. These Duret hemorrhages are believed to be caused by tearing of vessels that supply the upper brainstem [1]. Such hemorrhages are associated with rapid clinical decline and death. Fig. 1 Coronal section of the head showing particular areas of possible herniation: a subfalcine, b transtentorial, c tonsillar and d transcalvarial

Case 6 A 77-year-old woman with hypertension collapsed with an infarct of the right middle cerebral artery territory. This had resulted in uncal herniation with subsequent hemorrhagic infarction of the right posterior cerebral artery territory (Fig. 7).

Fig. 2 A glioblastoma multiforme of the left temporal lobe with midline shift and marked herniation of the cingulate gyrus beneath the falx cerebri (arrow)

123

262

Forensic Sci Med Pathol (2013) 9:260–264

Fig. 3 Subfalcine herniation viewed from above with the position of the falx marked by arrows and a dotted line

Fig. 4 Dissection of the cerebral hemispheres to show subfalcine herniation. The midline is marked by arrows

Case 7 Duret haemorrhages of the pons associated with raised intracranial pressure and uncal herniation (Fig. 8).

Tonsillar herniation This occurs when significantly elevated intracranial pressure from any cause results in herniation of the cerebellar tonsils through the foramen magnum, so-called ‘‘coning’’. At autopsy the acute situation can be recognized when the smooth herniated cerebellar folia are found with a

123

Fig. 5 Increased intracranial pressure in a 58-year-old man with right middle cerebral artery infarction causing marked bilateral uncal herniation with notching (arrows). The notching is more prominent on the right side

surrounding circular impression from the foramen magnum. Obstruction to the blood supply may cause infarction of the tonsils or parts of the medulla. Sloughed infarcted tissue may surround the upper cervical cord [4]. Chronic herniation occurs in Arnold–Chiari malformation where there is maldevelopment and downward displacement of portions of the medulla and cerebellum into the cervical spinal canal. This is associated with an increased incidence of sleep apnea and sudden death from brainstem compression [6].

Forensic Sci Med Pathol (2013) 9:260–264

263

Fig. 8 Typical Duret haemorrhages of the brainstem following elevation of intracranial pressure with uncal herniation

Fig. 6 A 76-year-old woman with a left intracerebral hemorrhage and marked notching of the left uncus and para hippocampal gyrus (arrow)

Case 8 Hemorrhagic infarction of the cerebellar tonsils following intracerebellar hemorrhage in a 70-year-old woman (Fig. 9). Secondary effects of tonsillar herniation include compression of the cervicomedullary junction which may compromise cardiorespiratory centers in the brainstem causing rapid death.

Transcalvarial hernation This occurs when elevated intracranial pressure forces brain tissue through craniotomy defects and has been referred to as Fungus cerebri, given the mushroom-like appearance of the herniated brain [7]. Case 9 Fungating cerebral cortex through bilateral burr holes in a 12-year-old girl with raised intracranial pressure from tuberculous meningitis (Fig. 10).

Fig. 7 Uncal herniation (arrow) with hemorrhagic infarction of the right posterior cerebral artery territory

In summary, increased intracranial pressure from a variety of causes may result in a range of cerebral herniations that are associated with specific, potentially lethal effects. Terminal mechanisms involve compression of vital centers or blood vessels with ischemia/infarction. Additionally, obstruction of cerebrospinal fluid pathways may compound the situation by contributing to an increase in intracranial pressure. Careful documentation of herniations at autopsy will enable a full analysis of the specific primary and secondary effects of a particular traumatic or organic condition.

123

264

Forensic Sci Med Pathol (2013) 9:260–264

Fig. 9 Tonsillar herniation with hemorrhagic necrosis

References 1. Frosch MP, Anthony DC, De Girolami U. The central nervous system. In: Kumar V, Abbas AK, Fausto N, Aster JC, editors. Robbins and Cotran pathological basis of disease. 8th ed. Philadelphia: Saunders Elsevier; 2010. p. 1279–344. 2. Byard RW, Gabriellian L, Helps SC, Thornton E, Vink R. Further investigations into the speed of cerebral swelling following blunt cranial trauma. J Forensic Sci. 2012. doi:10.1111/j.1556-4029. 2012.02109.x. 3. Fishman RA. Brain edema. New Engl J Med. 1975;293:706–11. 4. Leetsma JE. Forensic aspects of intracranial equilibria. In: Leetsma JE, editor. Forensic neuropathology. 2nd ed. Boca Raton: CRC Press; 2009. p. 343–98. 5. Pearce JM. Kernohan’s notch. Eur Neurol. 2006;55:230–2. 6. Byard RW. Mechanisms of sudden death and autopsy findings in patients with Arnold–Chiari malformation and ventriculoatrial catheters. Am J Forensic Med Pathol. 1996;17:260–3. 7. Gluckman J. Fungus cerebri—an unusual complication of mastoidectomy. SA Med J. 1975;49:1933–4.

Fig. 10 Fungus cerebri with cerebral herniation through two fronto parietal burr holes

123