FIGURE 11.3

Normal brain. (A) Neocortex. Triangular cells are neurons: their cytoplasm contains Nissl granules. The background is neuropil. (B) White matter. Myelinated white matter within which are oligodendroglia and a few astrocytes.

FIGURE 11.4

Neurons. (A) Left panel: normal motor neuron in ventral horn of spinal cord. The dark granules are the Nissl granules. The pale area is the region occupied by lipofuscin. Right panel: neurons showing the features of ischaemic cell change. They are shrunken and contain hyperchromatic nuclei, have intensely eosinophilic and luxophilic cytoplasm and may be decorated by incrustations. (B) Similar neurons showing the features of central
chromatolysis. Note the pale homogeneous cytoplasm and the eccentric nucleus.

FIGURE 11.5

Astrocytes. Reactive fibre-forming astrocytes that are both hypertrophied and hyperplastic. (Immunohistochemistry GFAP.)

FIGURE 11.6

Microglia. (A, B) The dark elongated nuclei represent the elongated nuclei of reactive microglia (rod cells). (C) Lipid-laden macrophages in a cerebral infarct. (B: immunohistochemistry CD68.)

FIGURE 11.7

Raised intracranial pressure, showing the intracranial compartments and the result of a mass lesion on the right hand side. In addition to a shift of the midline structures and distortion of the ventricular system, there is (A) a supracallosal (subfalcine) hernia; (B) a tentorial hernia; (C) a tonsillar hernia.

FIGURE 11.8

Raised intracranial pressure. The medial part of the temporal lobe has pushed medially and downwards to form a tentorial hernia. The deep groove (arrows) indicates the position of the edge of the tentorium. There is also secondary haemorrhage into the brainstem.

FIGURE 11.9

Cerebral contusions. The frontal and temporal lobes are affected by haemorrhagic contusions.

FIGURE 11.10

Diffuse traumatic axonal injury. There is a haemorrhagic lesion in the corpus callosum to the right of the midline. There are also gliding contusions (*) in the dorso-medial sectors of the hemispheres and a haematoma in the right thalamus. Note relative absence of superficial
contusions.

FIGURE 11.11

Diffuse traumatic axonal injury. There are many irregularly shaped axons and some bulbs in the corpus callosum. (Immunohistochemistry βAPP.)

FIGURE 11.12

Circle of Willis. The anterior part of the circle is derived from the internal carotid arteries which divide into the proximal portions of the paired middle and anterior cerebral arteries, and the posterior part of the circle is derived from the vertebral and basilar system which gives origin to the paired posterior cerebral arteries. The circle is completed anteriorly by the anterior communicating artery which joins the anterior cerebral arteries and posteriorly by the posterior communicating arteries, which join the posterior cerebral and internal carotid arteries.

FIGURE 11.14

Recent infarct in right cerebral hemisphere. The basal ganglia show the features of haemorrhagic infarction (reperfusion injury).

FIGURE 11.15

Cerebral infarction. There is a large infarct in the right cerebral hemisphere due to occlusion of the ipsilateral internal carotid artery. There are internal herniae and some asymmetry of the ventricles due to midline shift.

FIGURE 11.16

Cerebral infarction of several years’ duration. The necrotic tissue has been removed and the ipsilateral lateral ventricle is enlarged (compensatory hydrocephalus).

FIGURE 11.17

Diagram to show arterial boundary zones in the cerebral and cerebellar hemispheres. They lie between the territories supplied by the major arteries.

FIGURE 11.18

Intracerebral haemorrhage. There is a large haematoma in the basal ganglia due to chronic hypertension.

FIGURE 11.20

Subarachnoid haemorrhage. Due to rupture of a saccular aneurysm there are large amounts of recent haemorrhage in the basal cisterns. Dissection showed an aneurysm arising from the upper end of the basilar artery.

FIGURE 11.22

Tuberculous meningitis. (A) There is thick exudate at the base of the brain. (B) Within the meninges is a caseating granulomatous inflammatory process with Langhans’ giant cells.

FIGURE 11.23

Acute viral meningitis. The inflammatory cells (mainly around small blood vessels) are lymphocytes and plasma cells.

FIGURE 11.24

Acute viral encephalitis. Intracellular herpes simplex viral particles. (Electron microscopy.)

FIGURE 11.25

Encephalitis due to herpes simplex virus. Within the swollen right temporal lobe there are many small haemorrhagic foci. There is also a shift of the midline structures to the left.

FIGURE 11.26

Encephalitis due to herpes simplex virus. This patient survived for several weeks, severely brain damaged. The affected regions are now shrunken and focally cystic. The left temporal lobe is more severely affected than the right one.

FIGURE 11.27

HIV encephalitis. Multinucleated giant cells are a characteristic feature.

FIGURE 11.28

Multiple sclerosis. There are large grey plaques of demyelination in relation to the occipital horns of the ventricles.

FIGURE 11.29

Multiple sclerosis. (A) There is a plaque of demyelination in one dorsolateral sector of the pons. (B) Within the area of demyelination there is preservation of neurons and variable cuffing of blood vessels by lymphocytes. (Luxol fast blue/cresyl violet.)

FIGURE 11.32

Alzheimer’s disease. There is selective atrophy of the medial parts of each temporal lobe with associated compensatory hydrocephalus.

FIGURE 11.33

Alzheimer’s disease. There is a typical senile plaque composed of filamentous and granular material. A neurofibrillary tangle is seen in a neuron (arrow). (Kings amyloid stain.)

FIGURE 11.34

Huntington’s disease. The basal ganglia are markedly atrophied with a flattened outline compared with age-matched control. The cerebral cortex is also atrophied and compensatory hydrocephalus is a feature.

FIGURE 11.35

Creutzfeldt–Jakob disease. There is spongiform change in the cortex that is characterized by many vacuoles which become coalescent. Neuronal loss and astrocytosis are accompanying features.

FIGURE 11.36

(A) Sporadic Creutzfeldt–Jakob disease (CJD). Axial fluid attenuated inversion recovery (FLAIR) magnetic resonance (MR) image at level of basal ganglia in a patient with pathologically confirmed sporadic CJD showing symmetrical hyperintensity of the caudate head and anterior putamen (arrows). (B) New variant CJD. Axial FLAIR MR image at the level of the basal ganglia in a patient with pathologically confirmed variant CJD demonstrating bilateral hyperintensity of the pulvinar nucleus of the thalamus (arrows). (Courtesy of Professor I Bone, Department of Neurology, Southern General Hospital, asgow and Professor J W Ironside, Department of Neuropathology, Western General Hospital, Edinburgh.)

FIGURE 11.37

vCJD. Electroencephalogram. Non-specific slow wave activity. (Courtesy of Professor I Bone, Department of Neurology, Southern General Hospital, Glasgow and Professor J W Ironside, Department of Neuropathology, Western General Hospital, Edinburgh.)

FIGURE 11.38

CJD. (A) A florid plaque in the cerebral cortex formed of amyloid fibres of PrP. (B) Extensive accumulation of PrP in cortex. (A: H&E; B Immunohistochemistry PrP.) (Courtesy of Professor I Bone, Department of
Neurology, Southern General Hospital, Glasgow and Professor J W Ironside,
Department of Neuropathology, Western General Hospital, Edinburgh.)

FIGURE 11.39

Parkinson’s disease. (A) Compared with the normally pigmented substantia nigra on the left there is depigmentation of the substantia nigra on the right. (B) The Lewy body consists of a rounded eosinophilic inclusion which classically comprises a dense core surrounded by a pale halo.

FIGURE 11.41

Normal spinal cord.

FIGURE 11.42

Compression of the spinal cord. Metastatic carcinoma in the vertebral bodies is compressing the spinal cord.

FIGURE 11.43

The spinal cord above a transverse lesion. (A) Immediately above there is degeneration of the posterior columns and the spinocerebellar and the spinothalamic tracts. (B) Well above there is preservation of the cuneate tracts and there is less severe degeneration of the spinothalamic and spinocerebellar tracts.

FIGURE 11.44

Spinal cord below a transverse lesion. (A) There is degeneration in the corticospinal tracts. (B) There is degeneration in one corticospinal tract due to an old infarct in the internal capsule.

FIGURE 11.45

Fracture-dislocation of spine. Note haemorrhage into the intervertebral disc and associated spinal cord.

FIGURE 11.47

Glioblastoma. (A) There is a partly cystic necrotic tumour in the posterior frontal lobe that has remarkably well-defined margins. Associated brain swelling has produced internal herniation, ventricular asymmetry and a shift of the medial structures. (B) There are serpiginous foci of necrosis with surrounding nuclear pseudopalizading. The tumour is pleomorphic and multinucleate tumour giant cells, vascular endothelial cell hyperplasia and mitotic figures are present.

FIGURE 11.48

Glioblastoma. (A) Post-contrast CT scan, showing enhancement (black arrows), necrotic centre (white arrow) and mass effect. (B) Post-contrast CT scan, showing midline shift (black line is the midline of the cranial cavity, with the right frontal horn (black arrow) and the third ventricle (open arrow) on the left of the midline. (C) Post-contrast MRI scan, showing enhancement (black arrow), necrosis (white arrow) and swelling (open arrow). (D) Post-contrast MRI scan, showing probable extent of tumour cells. (Courtesy of Mr Papanastassiou, Department of  Neurosurgery, Southern General Hospital, Glasgow.)

FIGURE 11.49

Meningioma. (A) The tumour arising from the base of the skull has produced a depression in the undersurface of the frontal lobes from which it can be readily withdrawn. (B) There are whorls of cells some of
which are calcified – psammoma bodies.

FIGURE 11.50

Schwannoma. (A) A cerebellopontine angle mass that has distorted related structures and has induced a degree of obstructive hydrocephalus. (B) In addition to closely packed elongated cells, there are more loosely arranged cells.

FIGURE 11.51

Metastatic tumour. (A) Horizontal slice of brain in which there are multiple metastases. (B) Interface between brain tissue and deposit of metastatic melanoma.

FIGURE 11.52

Malignant meningitis. (A) Cytospin preparation that shows many large malignant cells with nuclear pleomorphism and multiple nucleoli and a mitosis. (B) Cytospin preparation immunoreacts with epithelial marker confirming metastatic carcinoma (same case as A). (A: Leishman; B: immunohistochemistry cytokeratin.)

FIGURE 11.53

(A) Structures of the anterior segment of the eye, and the principal route of aqueous flow. (B) Structures of the posterior segment of the eye, and vascular supply to the choroid, retina and optic disc.

FIGURE 11.54

Shrinkage and disorganization of the eye following inflammation (phthisis bulbi). The retina is detached and entrapped within fibrous tissue. There is osseous metaplasia (arrow). Low pressure has resulted in an exudate (E) in the suprachoroidal space.

FIGURE 11.55

Optic nerve in glaucoma. (A) Normal optic disc for comparison. (B) Atrophic nerve head giving rise to ‘cupping’ seen in advanced glaucoma.

FIGURE 11.56

Malignant melanoma of the choroid. (A) This large tumour shows both pigmented and non-pigmented areas and has pushed the lens forward causing closure of the chamber angle (arrow) with secondary glaucoma. (B) Histology of this tumour shows large epithelioid cells (e) and spindle cells (s). Some of the cells contain brown melanin pigment (arrow).

FIGURE 11.57

Retinoblastoma. (A) This large white tumour is in continuity with the retina (r). There is focal calcification within the tumour (arrow). (B) Histology of this tumour shows typical rosettes (r) as well as numerous apoptotic bodies (arrows).