58 DAVID SUTTON PICTURES INTRACRANIAL LESIONS (2)

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58INTRACRANIAL LESIONS (2)

DAVID SUTTON 58.23

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

• Fig. 58.1 (A) Massive capsular haematoma with blood in the ventricles. (B) Spontaneous haemorrhage into right fontal lobe, minor extension into right lateral ventricle. Low density around haematoma due to clot retraction.

• Fig. 58.2 (A) Axial unenhanced CT and (B) T2 -weighted MR image demonstrating an acute intrinsic pontine haemorrhage.

• Fig. 58.3 CT of resolving left thalamic haemorrhage 10 days after onset. (A) Before contrast there is some residual high density centrally. (B) After contrast there is marginal enhancement.

• Fig. 58.4 (A) MR of subacute posterior fossa haemorrhage. T 2 -weighted, and 3 4 days after onset. Low signal lesion with some marginal high signal. (B) MR T2-weighted, and 3-4 days after onset. Low-signal lesion with some marginal high signal. (B) MR (T 2 -weighted). Large haematoma in right temporal lobe 10 days after ictus. Peripheral high signal (C) MR (T2 -weighted). Cortical haematoma at 4 weeks. Note rim of low density.

• Fig. 58.5 (A) Subarachnoid haemorrhage. Congealed blood in the basal cisterns, insulae and interhemispheric cleft. (B) Clot in both frontal lobes from anterior communicating ruptured aneurysm. (C) Subarachnoid haemorrhage from right middle cerebral aneurysm. In addition to blood in the subarachnoid space, there is a local clot in the anterior part of the right insula indicating the site of the ruptured aneurysm. (D) Ruptured anterior communicating aneurysm with blood between frontal lobes, in septal cyst and in ventricles.

• Fig. 58.6 (A) Enhanced CT shows a right posterior communicating aneurysm. (B) Large irregular suprasellar aneurysm after enhancement. (C) High-density rounded mass in suprasellar region. (D) The mass enhances strongly with contrast medium. Large aneurysm confirmed at angiography (L36, W80).

• Fig. 58.7 (A) MRA axial study. Large aneurysm of the right carotid artery bifurcation is shown protruding up from the right cavernous sinus. There is also a small occipital angioma supplied by the right posterior cerebral artery. (B) Axial T 2- weighted MR image showing a small anterior communicating artery aneurysm. (C) Axial T2 -weighted MR showing a small aneurysm of the distal left posterior cerebral artery.

• Fig. 58.8 (A,B) Basilar aneurysms confirmed at angiography. Two different patients with high-density enhancing rounded masses behind the sella and extending into brainstem. (C) MRA shows left posterior communicating aneurysm. (D) Giant right intracavernous carotid aneurysm (3D MRA, TOF). (E) Lateral (a) and (b) views of giant basilar tip aneurysm. Flow arches up and over the invisible main cavity. (F) MRA (compressed axial 3D TOF). Two angiomas, one temporo-occipital, one anterior temporal. (G) MRA (3D TOF). Occluded right internal carotid artery cross-filling from left to right.

• Fig. 58.9 (A) Axial MR section (T2 -weighted) at base of skull. The right carotid and both vertebrals (lateral to the cord) show no signal due to normal flow. The dilated left internal carotid shows dissection with high signal in the false channel due to low or no flow (arrow). (B) CT with coronal reformat shows kinked vertebral artery arching high into left cerebellopontine angle (arrows) and compressing 7th nerve in a patient with facial tic.

• Fig. 58.10 (A) Large temporal angiomatous malformation. Note mottled appearance. The dilated vessels are of slight increased density and there are small 'cystic' and low-density areas. (B) After contrast medium, the dilated serpiginous vessels are well shown. Major drainage is to an aneurismal vein of Galen. (C) Large occipital angioma. CT shows mottled area of mixed high and low densities with flecks of calcification. (D) After enhancement multiple dilated vascular shadows are shown.

• Fig. 58.11 Patient with proptosis and orbital bruit due to dural AV fistula. CT shows grossly dilated superior ophthalmic vein.

• Fig. 58.12 (A,B) MR T 2 -weighted image shows an angioma lying with tortuous vessels mainly in the left temporal lobe.

• Fig. 58.13 MR study (T,-weighted). (A) Midline sagittal section. (B) Axial section. A large complex midline angioma drains into an aneurismal vein of Galen, and there is a dilated straight sinus and aneurysmal torcular. (C) MR study (T,-weighted). Right temporoparietal angioma supplied by hypertrophied middle cerebral artery. (D) Coronal MR study (T,-weighted) of small left parasagittal angioma showing cone-like extension into brain.

• Fig. 58.14 (A,B) Extensive bilateral AVMs are demonstrated on these two axial T 2 -weighted MR images. There are multiple enlarged superficial drainage veins. (C) Axial MR shows transpontine venous angioma. (D) Angiogram shows abnormal drainage veins.

• Fig. 58.15 (A) Sagittal midline MR (TI-weighted). Cavernous angioma of pons appears as in homogeneous mixed-signal lesion with peripheral low-signal halo. (B) Axial section (T]-weighted) shows the lesion equally well. (C,D) Axial MR scans T2 -weighted show large haematoma, which showed cavernomatous features on histology, on the right frontal lobe.

• Fig. 58.16 CT shows watershed infarct at junction of LMCA and ACA territory.

• Fig. 58.17 CT shows basal ganglia calcification in a child with HIV/AIDS. There are also small established vascular infarcts, the largest in the right frontal region.

• Fig. 58.18 Acute infarct. (A) Doubtful low-density in the left occipital region. No mass effect. (B) Strong enhancement with contrast medium. (C) Middle cerebral infarct. Mixed low-density and isodense lesion in right parietal region. No mass effect. (D) Patchy enhancement after contrast medium.

• Fig. 58.19 (A,B) MR axial sections showing infarcts in two different patients (A) T2 -weighted. Right cerebellar infarct appears as high signal. (B) T1-weighted. Large areas of low signal in both hemispheres from embolic infarcts in a patient with hypertrophic cardiomyopathy. (C,D) MR axial sections (T]-weighted) showing high signal from sagittal and transverse sinuses which are thrombosed.

Fig. 58.19 (A,B) MR axial sections showing infarcts in two different patients (A) T2 -weighted. Right cerebellar infarct appears as high signal. (B) T1-weighted. Large areas of low signal in both hemispheres from embolic infarcts in a patient with hypertrophic cardiomyopathy. (C,D) MR axial sections (T]-weighted) showing high signal from sagittal and transverse sinuses which are thrombosed.

• Fig. 58.20 (A) Axial section shows thrombosed right transverse sinus with evidence of venous infarcts in temporal lobe. (B) Left cavernous sinus occluded shows high signal around patent internal carotid; axial MR section shows left proptosis.

• Fig. 58.21 MRA shows occlusion of left internal carotid at its origin.

• Fig. 58.22 MRA shows atheromatous irregularity of proximal segments and trifurcation.

Fig 58.23 (A) Axial MR T-weighted child with AIDS mature right ACA 2 - and right MCA territory infarcts show as high-signal. (B) Axial MR T 2 increased signal.

• Fig. 58.24 (A,B) Perfusion MR. Occlusion of right internal carotid artery.

• Fig. 58.25 Diffusion MR shows recent small left frontal cortical infarct.

• Fig. 58.26 (A) MRI shows large area of right hemisphere with high signal. (B) MRA shows occlusion of right internal carotid artery.

• Fig. 58.27 (A) Acute extradural haematoma. High-density biconvex mass in right occipitoparietal region with mass effect following trauma (L34, W75). (B) Acute subdural haematoma. Superficial high-density concavoconvex lesion (arrows) with marked mass effect.

• Fig. 58.28 Subdural haematoma 3 weeks after onset. The clot is largely absorbed and the subdural fluid is now of low density.

Fig. 58.30 (A) Isodense subdural. Note mass effect and effacement of sulci which suggest diagnosis prior to contrast medium. (B) Post enhancement scan of another isodense subdural. The lesion stands out against the enhanced surface of the brain.

• Fig. 58.31 (A) Subcortical traumatic haematoma. (B) Haemorrhagic contusions in right frontal region. (C-D) Multifocal haemorrhages and contusions in both hemispheres.

• Fig. 58.32 (A,B) Cerebral trauma. Contusions in left temporal lobe. (C) Subcortical small haemorrhages associated with shearing injury, and a few large haemorrhages. (D) Head injury in a child. There is cerebral oedema mainly on the right, associated with compression of the ventricles and some shift to the right.

• Fig. 58.33 (A) Depressed fracture in the left temporal region with underlying haemorrhagic contusions (134, W75). (B) Same case at higher level (L) to show bone detail (L128, W75). (C) Frontal aerocele. (D) Bone window film showing frontal fracture and connection with top of frontal sinus.

• Fig. 58.34 Subdural haematoma shown by MR (T1-weighted) as high signal overlying left hemisphere. (A) IR 1400/400 (B) SE 1400/40 (Courtesy of Dr Graeme Bydder).

• Fig. 58.35 Post-traumatic porencephalic cyst or encephalomalacia. Large cortical and subcortical defect in the left frontal region several years after a severe head injury.

• Fig. 58.36 CSF fistula. CT cisternography. Direct corona) sections with patient prone. Soft tissue (A) and bone (B) window. Contrast medium has entered an empty sella. Pituitary stalk is arrowed. Bone window shows level of contrast fluid in the sphenoid sinus on the left.

• Fig. 58.37 (A,B) Cerebral abscess. (A) Low-density lesion in occipital region with some mass effect. (B) After contrast medium, note thin ring of enhancement round the abscess with oedema anteriorly. (C) Multiple abscesses in frontoparietal area showing capsular enhancement after contrast medium (L34, W75). (D) Capsular enhancement in bilocular abscess. (E,F) Otogenic abscess in left posterior temporal region with thick enhancing capsule and oedema posteriorly.

Fig. 58.38 (A) Axial T2 - weighted image of a left parietal abscess and associated vasogenic oedema. The central contents are hyperintense but the low-signal rim is thought to be secondary to the paramagnetic effects of the free radicals present. (B) Axial post-contrast CT in a child demonstrating bilateral low-density subdural empyemas with enhancement of the inner membranes.

• Fig. 58.39 Tuberculoma. (A) Isodense lesion with surrounding oedema. on T, weighted images. The lesion now shows ring-enhancement (B) Mixed enhancement after contrast. (C) Tuberculomas. Two small lesions with thick ring enhancement ([40, W80). (D) Small brainstem tuber- on both CT and MRI and perilesional oedema remains. The radioculomas with ring enhancement anterior to dilated fourth ventricle.

• Fig. 58.40 Tuberculomas in right frontal region with nodular enhancement (A) and upper midbrain with ring enhancement (B). (C) Sagittal reformat of midbrain lesion. Note infundibulum and pituitary gland well shown.

• Fig. 58.41 Axial T2 -weighted image (A) showing a hypo intense caseating tuberculous granuloma in the right frontal lobe in association with vasogenic oedema. The lesion is situated at the grey-white matter junction and on the postcontrast T, axial image (B) has a multiloculated ring enhancing appearance.

• Fig. 58.42 An irregular enhancing tuberculoma is shown within the pons on the postcontrast axial T,-weighted MR image. (A) The lesion is of relatively low signal on the T2 axial image (B) and there is extensive vasogenic oedema and some modest mass effect with distortion of the 4th ventricle. Axial T 2 -weighted MR (C) demonstrating third and lateral ventricular hydrocephalus with transependymal oedema around the occipital horns. This was secondary to tuberculous meningitis. On the coronal T, postcontrast image (D) there is nodular meningeal thickening and enhancement around the brainstem and cerebellum.

• Fig. 58.43 (A,B) Bilateral basal ganglia cryptococcomas, which have a slightly punctuate appearance on the T 2 -weighted images. On the T, coronal images, the lesions are slightly hypointense and those on the right exert some mass effect on the right frontal horn. (C,D) Axial and coronal sections T2-weighted and T,-weighted show small enhancing abscess impinging on the right ventricle.

• Fig. 58.44 (A,C) Congenital toxoplasmosis. Grossly dilated ventricles and calcified granulomas in atrophic cortex and basal ganglia.

• Fig. 58.45 (A) Toxoplasmic encephalitis in a patient with AIDS. Multiple small abscesses with ring enhancement. A ring enhancing lesion proven to be a toxoplasmosis abscess is shown peripherally in the left frontal lobe on the T2 axial (B) and T, coronal postcontrast image (C). The appearances are non-specific and there is a large amount of associated vasogenic oedema. Multiple small enhancing nodules are present predominantly at the grey-white matter junction in this T, axial image (D). The associated perilesional oedema is clearly seen on the T 2 axial image (E); this patient was known to have AIDS and these were multiple toxoplasmosis abscesses. on the degree of brain destruction caused by the infection. There

• Fig. 58.46 Enhanced CT in acute cysticercosis. (A) Multiple ring and nodular lesions inconstantly accompanied by oedema. (B) Another patient with chronic quiescent cysticercosis. The brain was riddled with cysts and calcified nodules. (C) The axial T 2- weighted MR in this patient who presented acutely with epileptic seizures showed a small hypointense lesion in the medial right temporal lobe associated with a small amount of vasogenic oedema. (D) On the postcontrast T, coronal image, this lesion showed almost uniform enhancement and resolved on treatment for cysticercosis.

• Fig. 58.47 Huge hydatid cyst in the left frontal lobe. It is of CSF density and shows no capsular enhancement of adjacent oedema. It expands the overlying skull vault.

• Fig. 58.48 Multiple TZ hyperintense lesions in the basal ganglia, thalami, internal capsules and periventricular white matter are present in this patient with acute disseminated encephalomyelitis (ADEM).

• Fig. 58.49 Herpes encephalitis. (A) Lowdensity area in right temporal region with slight mass effect. (B) Bilateral low-density areas in both temporal lobes. Burr hole for brain biopsy on right. (C) After contrast medium there is marked irregular enhancement, mainly gyral.

Fig. 58.49 Herpes encephalitis. (A) Lowdensity area in right temporal region with slight mass effect. (B) Bilateral low-density areas in both temporal lobes. Burr hole for brain biopsy on right. (C) After contrast medium there is marked irregular enhancement, mainly gyral.

• Fig. 58.50 MR (T,-weighted) shows high signal in both temporal lobes. Herpes encephalitis.

• Fig. 58.51 Progressive multifocal leucoencephalopathy. (A) Occipital lesions mainly on right. (B,C) Several weeks later, the disease has progressed through both hemispheres but most markedly on the right. Multifocal well-defined hyperintense lesions confined to the white matter are shown on this T,-weighted axial image (D) of an immunocompromised patient. The signal abnormality extends into the gyral cores. The left frontal lesion shown on the T, coronal postcontrast image (E) is markedly hypointense, non-enhancing and despite its size is not associated with any mass effect. These lesions are typical of progressive multifocal leucoencephalopathy (PML).

• Fig. 58.52 (A) Axial T2 -weighted image in a patient with AIDS showing widespread signal abnormality in the white matter of HIV encephalitis. There is also background atrophy with ventricular enlargement and mild sulcal widening. (B) AIDS encephalitis.

• Fig. 58.53 (A) Axial MR section with gadolinium enhancement (T,-weighted) shows superficial peduncular lesions (arrows). Sarcoidosis. (B) Intracanalicular optic neuritis secondary to sarcoid. Left optic nerve shows high signal on T,-weighted MR. (C) Sarcoidosis with marked meningeal thickening.

• Fig. 58.54 Generalised atrophy. (A) Dilated lateral ventricle. (B) Enlarged sulci and interhemispheric fissure (L36, W80).

• Fig. 58.55 (A-D) Communicating hydrocephalus complicating meningitis. All four ventricles are dilated and the sulci are effaced.

• Fig. 58.56 (A) Alzheimer's disease. Coronal MRI showing bilateral symmetrical atrophy of each hippocampus and parahippocampal gyrus. (B,C) Frontotemporal dementia (non-Pick). Coronal MRI showing severe atrophy of the anterior part of the left temporal lobe and mild enlargement of the frontal horn of the left lateral ventricle. (D) True Pick's disease, showing more mild left temporal lobe atrophy.

• Fig. 58.57 T2- weighted axial images in a patient with CADASIL (cerebral autosomal dominant arteriopathy, subcortical infarcts and leucoencephalopathy) showing predominantly confluent signal hyperintensity in the cerebral white matter, fairly symmetrical in distribution. The changes are particularly marked in the temporal lobes (A). The basal ganglia also exhibit a lacunar state (B).

Fig. 58.58 Axial T2 – weighted image in a patient with multisystem atrophy showing marked atrophy of the pons and middle cerebellar peduncles. Abnormal T2 high signal is present in the pons in the form of a cross (hot cross bun sign) with more confluent signal hyperintensity in the middle cerebellar peduncles. The cerebellum is also atrophic and the 4th ventricle is consequently enlarged.

• Fig. 58.59 Cerebellar atrophy showing widened sulci and fissures. The brainstem is also atrophic.

• Fig. 58.60 T2-weighted axial images demonstrating basal ganglia, thalamic and midbrain lesions in Wilson's disease.

• Fig. 58.61 Calcification of the basal ganglia.

• Fig. 58.62 Axial CT scans demonstrating extensive calcification in the basal ganglia, thalami, subcortical white matter, brainstem and dentate nuclei of the cerebellum in Fahr's syndrome.

• Fig. 58.63 Axial T 2- and T,-weighted images in Cockayne's syndrome demonstrating gross supratentorial atrophy and diffuse signal abnormality and reduction in bulk of the white matter. T, high and Tz low signal in the basal ganglia is indicative of calcification.

• Fig. 58.64 Multiple sclerosis. (A) Paraventricular and white-matter low-density areas. (B,C) Enhancing paraventricular and white-matter low-density areas. (D) Axial MRI section J, -weighted). Multiple sclerosis plaques are seen as areas of high signal.

• Fig. 58.66 (A-C) Axial CT scans demonstrating confluent and symmetrical low-density change in the deep and peripheral supratentorial white matter in metachromatic leucodystrophy. (D) Axial MR Tz W shows widespread low density in white matter.

• Fig. 58.69 (A) Axial T2 and (B) T, coronal postcontrast images in a patient with Alexander's disease showing signal abnormality in the white matter, which has a predilection for the frontal lobes. There is some basal ganglia involvement and enhancement postcontrast.

• Fig. 58.70 (A) Axial T2 -weighted MRI showing bilateral parietal periventricular signal abnormality in a patient with classical phenylketonuria. (B) Axial CT showing extensive very low density change in the cerebral white matter and thalami in maple syrup urine disease.

• Fig. 58.71 (A) Multiple dilated perivascular spaces are present on the T 2 -weighted axial image in this patient with mucopolysaccharidoses. (B) Tz sagittal image through the craniocervical junction in Morquios' syndrome showing a small foramen magnum and some cervical cord impingement. There is odontoid hypoplasia and ligamentous and dural thickening contributing to the small foramen magnum.

• Fig. 58.72 (A,B) CT of elderly demented patient. Cortical atrophy is mild but there are extensive areas of patchy low density in the deep cerebral white matter. Binswanger's disease.

• Fig. 58.73 (A) Axial T2- and (B) coronal T1 -weighted images showing extensive signal abnormality in the cortex and white matter of the right cerebral hemisphere in MELAS. There is some mass effect and note that the signal change involves all three vascular territories, although is largely posterior in distribution. There is also cerebellar atrophy.

• Fig. 58.74 Bilateral mature cystic cleft-like lesions have occurred in the lentiform nuclei in this patient with a mitochondrial cytopathy. (A) Axial MR T2 W. (B) Coronal MR T2 W.

• Fig. 58.75 Mitochondrial cytopathy. Four-year-old boy with ataxia, myoclonus and drowsiness. MRI (T 1 -weighted) reveals loci of high signal in the lentiform nuclei and parietal white matter extending into posterior limbs of internal capsule.

• Fig. 58.76 (A) Diagram of hippocampus and its relationships. A. Lateral aspect of left temporal lobe. B-E Coronal sections from before backward at levels shown in A. Ch F = choroidal fissure; F = fimbria; MD = margo denticulatus (dentate gyrus); HFi = hippocampal fissure; TH = temporal horn; CAI = four regions within hippocampus itself; PHG = parahippocampal gyrus; UN = uncus; EC = entorhinal cortex; UG = uncinate gyrus; SLG = semilunar gyrus (part of amygdala); GA = gyrus ambiens; HF = hippocampal formation; OF = uncal fissure; CS = collateral sulcus; UN = uncal notch; SUB = subiculum. (B) Coronal MRI section through left medial temporal lobe at level of C above. T,-weighted.

• Fig. 58.77 (A) Corona) MRI sections, T2 -weighted, through hippocampal bodies, corresponding to level E of Fig. 58.76A. The left hippocampus is smaller than the right and shows higher signal. Hippocampal sclerosis. (B) Coronal MRI (FLAIR) image at level of hippocampal body accentuating high signal in left hippocampus. (C) T,-weighted image at similar level from a 3D accumulation, showing the left hippocampus to be much smaller than the right.

• Fig. 58.78 Coronal MRI (T 2 -weighted). Abnormal vessels are shown in the right medial temporal lobe involving the hippocampus. Angioma.

• Fig. 58.79 Diagram showing three standard sagittal sections (A) and six coronal sections (B).

• Fig. 58.80 A coronal section in the third position showing the bodies of the lateral ventricles (V) and the sylvian fissures (SF). Lying between the lateral ventricles is the cavum septi pellucidi (CSP).

• Fig. 58.81 A coronal section in the fourth position showing the prominent landmark of the parahippocampal gyri (HG). V = lateral ventricles.

• Fig. 58.82 A coronal section in the sixth position showing the characteristic echogenic choroid plexus (CP).

• Fig. 58.83 A sagittal section in the midline showing the echogenic cerebellum and the fourth ventricle (arrow) posteriorly.

• Fig. 58.84 An angled sagittal section showing the full sweep of one lateral ventricle around the caudate nucleus and thalamus.

• Fig. 58.85 (A) A coronal section showing the typical appearance of hydrocephalus involving the lateral and third ventricles. The section is through the foramen of Monro. Echogenic haemorrhage is within the ventricle. (B) A ventricular shunt in position more posteriorly.

• Fig. 58.86 (A) A coronal section. (B) A sagittal section showing the characteristic findings of the Dandy- Walker syndrome. There is cystic dilatation of the fourth ventricle filling the posterior fossa. A shunt is in place.

• Fig. 58.87 (A) A coronal section. (B) A sagittal section showing the findings of a retrocerebellar arachnoid cyst for comparison. Note that in the sagittal section the cerebellum (Cb) and the fourth ventricle (iv) can be seen compressed forward by the cyst.

• Fig. 58.88 Coronal section showing the single fused ventricle typical of holoprosencephaly.

• Fig. 58.89 A coronal section in a premature infant showing a typical reflective haemorrhage (H) from the germinal matrix. A mass effect from the haemorrhage is distorting and elevating the lateral ventricle on this side.

• Fig. 58.90 A posterior coronal section showing asymmetric enlargement of one choroid plexus (H) typical of haemorrhage.

• Fig. 58.91 A sagittal section showing the characteristic appearances of advanced periventricular leucomalacia (PML) as periventricular cystic spaces.

• Fig. 58.93 A transcranial section showing a large crescentic subdural haematoma.

• Fig. 58.94 99 "Tc-exametazime brain SPECT: axial (A), Coronal (B), right parasagittal (C) and left parasagittal (D) sections in a patient with massive infarction of the right middle cerebral artery territory. Note severe ischaemia o5 the Srontai, tempura% and panetai cortex and also oI the basal ganglia on the right.

• Fig. 58.95 99 ", Tc-exametazime brain SPECT: axial, coronal and right parasagittal images showing very extensive perfusion deficits during the acute ischaemic phase (top row) and substantial improvement several months later after clinical recovery (bottom row).

• Fig. 58.97 19mTc-exametazime brain SPECT: axial (top row) and left and right parasagittal (bottom row) sections in a patient with suspected Alzheimer's disease. The distribution is primarily posterior but quite asymmetric, unlike Fig. 58.96.

• Fig. 58.99 99 -Tc-exametazime brain SPECT: axial (top row) and left and right parasagittal (bottom row) sections in a patient with dementia of frontal lobe type. Note the marked frontal and temporal ischaemia with central atrophy as well.

58 DAVID SUTTON PICTURES INTRACRANIAL LESIONS (2)

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