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Radiological pathology of Hereditary ataxias
Feb 10th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

February 10, 2012 — Radiological pathology of Hereditary ataxias

In this topic Professor Yasser Metwally discusses the pathology and pathogenesis of Hereditary ataxias and its radiological picture.

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Lecture 1. View topic online…Topic of the month: Radiological pathology of Hereditary ataxias

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  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) yassermetwally.com corporation, version 14.1 January 2013 [Click to have a look at the home page]

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Intravascular malignant lymphomatosis
Feb 2nd, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

February 2, 2012 — The intravascular malignant lymphomatosis (IML), also known as angiotropic large cell lymphoma, represents only 3% of the non-Hodgkin lymphomas and affects middle-aged and elderly patients (median 61 years) with a cerebral manifestation in 74% of the individuals. Signs of dementia or disorientation are reported in the literature in 53% and seizures in 25% of patients (1,3). Important features in intravascular malignant lymphomatosis (IML), are the symmetrical involvement of the temporal lobes and the cingulate gyri that might be misdiagnosed as limbic encephalitis. The prognosis of IML is poor with a median survival time of only 6 months after symptom onset. Temporary remission to a maximum of a few weeks is described in patients who received corticoids or cytostatic drugs (3).

Click to enlarge figure

Figure 1. MRI in a case of intravascular malignant lymphomatosis revealed in T2-weighted images hyperintense lesions bilaterally in both temporal lobes, the right occipital white matter and in the region of the cingulate gyrus

The key microscopic feature of IML is the filling of lumina of small and medium-sized vessels with large atypical lymphoid cells. These cells possess predominantly round nuclei, vesicular chromatin and prominent nucleoli. Mitotic figures are common. Immunohistochemically, these cells are positive for leukocyte common antigen and usually B cell markers, but a few cases of T cell origin have been described. The blood vessels are closed and sometimes thrombosed by tumor cells leading to circulation disturbances resulting in multiple, ischemic microinfarctions as well as small parenchymal hemorrhages. Endothelial proliferation may be present (4). Migration out of the vascular spaces is rarely seen and this is likely due to the lack of surface expression of leukocyte adhesion molecule CD11a/CD18 by the tumor cells (2). Securing the diagnosis by brain biopsy is controversial, however, brain biopsy confirmed the diagnosis in 50% of individuals with brain involvement. While skin biopsy is more convenient, dermal involvement is sufficiently low to miss the diagnosis in 2/3 of all patients (3). Consequently, brain biopsy is recommended as the preferable way to establish this diagnosis.

In conclusion, in a case of dementia, seizures and infarct-like lesions by MRI, the diagnosis of an intravascular malignant lymphomatosis should be considered.


References

  1. Chapin, J.E., Davis, L.E., Kornfeld, M., Mandler R.N. (1995) Neurologic manifestations of intravascular lymphomatosis. Acta Neurol Scand 91: 494-499.

  2. Jalkanen, S., Aho R., Kallajoki, M., Ekfors, T., Nortamo, P., Gahmberg, C., Duijvestijn, A., Kalimo, H. (1989) Lymphocyte homing receptors and adhesion molecules in intravascular malignant lymphomatosis. Int J Cancer 44: 777-782.

  3. Teves, T.A., Gadoth, N., Blumen, S., Korczyn, A.D. (1995) Intravascular Malignant Lymphomatosis: A Cause of Subacute Dementia. Dementia 6: 286-293.

  4. Warnke, R.A., Weiss, L.M., Chan, J.K.C., Cleary, M.L., Dorfmann, R.F. (1995) Atlas of Tumor Pathology, Tumors of the Lymph Nodes and Spleen. Third Series, Fascicle 14, Armed Forces Institute of Pathology, Washington.

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Lacunar infarcts
Jan 12th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

January 12, 2013 —  Lacunar infarcts or lacunes are small, deep cerebral infarcts involving the penetrating arteries that supply the basal ganglia, internal capsule, thalamus, and brainstem. These small arteries arise from the major cerebral arteries and include the lenticulostriate branches of the anterior and middle cerebral arteries, the thalamoperforating branches of the posterior cerebral arteries, and the paramedian branches of the basilar artery. These penetrating arteries are small end arteries (100-500 m in diameter) that are difficult to evaluate angiographically. Most of these arteries are unbranching single vessels with essentially no collateral circulation. For these anatomic reasons, deep lacunar infarcts typically are spherical in shape and range from 0.3 to 2.5 cm in diameter. The larger lacunes typically result from more proximal obstructions.

Lacunar infarcts are commonly seen in patients older than 60 years with hypertension. Because this population is also prone to chronic small vessel disease, identification of small recent lacunar infarcts superimposed on chronic disease can be difficult. Diffusion imaging is extremely helpful in acute and early subacute infarcts in this regard. Contrast enhancement is likewise extremely helpful in identifying late subacute infarcts.

The pathogenesis of lacunar infarction is as follows. Chronic hypertension causes degeneration of the tunica media (i.e., arteriosclerosis), with hyalin deposition in the artery wall that narrows the lumen. Plaque or thrombosis, called microatheroma, may subsequently occlude these vessels, particularly the larger vessels. The weakened tunica media also predisposes to the formation of microaneurysms, which can rupture, causing an intraparenchymal hematoma. A hypertensive hemorrhage or hypertensive hemorrhagic infarction has a characteristic location in the deep cerebral structures supplied by these deep penetrating arteries. Other uncommon causes of lacunar infarction include secondary arteritis caused by meningitis, microemboli, and arterial dissection.

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Figure 1. Early subacute lacunar infarction involving the posterior limb of the left internal capsule. Vasogenic edema is noted (with abnormal high signal intensity) on the T2-weighted fast spin echo (A) and fluid-attenuated inversion recovery (B) scans. There is corresponding abnormal low signal intensity on the postcontrast T1-weighted scan (C). However, there is no abnormal contrast enhancement (with disruption of the blood-brain barrier yet to occur). The mean transit time (MTT) for the lesion is prolonged, as seen on a calculated MTT image (D) from a first-pass perfusion study. E, Diffusion weighted imaging and the apparent diffusion coefficient map (F) reveal the presence of cytotoxic edema, as would be anticipated in an infarct less than 1 week old.

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Figure 2. Late subacute lacunar infarction involving the posterior limb of the right internal capsule. The patient is an elderly diabetic who presented with acute hemiparesis. The magnetic resonance exam was obtained 10 days after presentation, at which time the hemiparesis had resolved. Multiple high signal intensity abnormalities are noted bilaterally on the T2-weighted scan (A). The postcontrast T1-weighted scan (B) reveals punctate enhancement (arrow) in the posterior limb of the right internal capsule. This corresponds to a high signal intensity lesion on the T2-weighted scan. By identification of abnormal contrast enhancement, this subacute infarct can be differentiated from other chronic ischemic lesions, which are incidental to the patient’s current medical problems.

Lacunar infarction is often recognized by a distinctive clinical presentation. A pure motor stroke is the most common clinical syndrome, accounting for 30% to 60% of lacunar infarcts. A pure sensory stroke, combined sensorimotor stroke, ataxic hemiparesis, dysarthria (or ”clumsy hand syndrome”), and brainstem syndromes are other characteristic clinical presentations of lacunar infarction. Patients with lacunar infarction often have a gradual progression of symptoms. An antecedent TIA occurs in approximately 25% of patients with lacunar infarction.

On MRI, lacunar infarcts appear as focal slit-like or ovoid areas of increased water content. They are high signal intensity on T2-weighted images and isointense to low signal intensity on T1-weighted images. T2 -weighted scans are more sensitive than T1 – weighted scans for detection. In acute lacunar infarction, vasogenic edema may not be present; thus, diffusion- weighted scans are important for detection. Fluid-attenuated inversion recovery (FLAIR) scans are helpful in identifying small lacunes and differentiating them from spaces containing cerebrospinal fluid (CSF). If FLAIR is not an option, then spin echo scans with intermediate T2-weighting provide similar information. On either type of scan, lacunar infarcts appear as small high-signal intensity focal lesions and can be easily distinguished from the intermediate to low signal intensity of normal surrounding brain and CSF. MRI is much more sensitive than CT in detecting lacunar infarcts. Contrast enhancement of subacute lacunar infarcts, after intravenous gadolinium chelate administration, is consistently seen on MRI. Enhancement occurs as a result of blood-brain-barrier disruption. Chronic lacunar infarcts are characterized by focal cavitation and a more pronounced decreased signal intensity on T1-weighted images than in the earlier stages of lacunar infarction. These chronic (cavitated) lacunar infarcts are isointense with CSF on all imaging sequences.

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Figure 3. Early subacute thalamic infarction. A, Two round lesions, with abnormal high signal intensity corresponding to vasogenic edema, are noted medially on the T2-weighted scan. The smaller lies in the right thalamus, the larger in the left thalamus. There is subtle low signal intensity in the corresponding areas on the T1-weighted precontrast scan (B). There was no abnormal contrast enhancement (not shown). Thalamic lesions are easily missed by inexperienced film readers, leading to the recommendation that the thalamus be visually checked for abnormalities on each scan.

Textbook-of-neuroimaging...MRI-appro[26]

Figure 4. Early subacute bilateral pontine infarction. The central portion of the pons has abnormal high signal intensity on the T2- weighted scan (A) and abnormal low signal intensity on the T1-weighted scan (B). Despite the lesion being bilateral, there is some indication of a straight border along the midline. A follow-up T1-weighted scan (C) performed 6 months later demonstrates cavitation of the lesion.

Textbook-of-neuroimaging...MRI-appro[10]

Figure 5. Late subacute pontine infarction. On the precontrast T2- weighted scan (A), an area of abnormal hyperintensity is noted in the left pons, with a sharp line of demarcation along the median raphe. The lesion enhances on the postcontrast T1-weighted scan (B). As with other lacunar infarcts, pontine infarcts will consistently demonstrate contrast enhancement after gadolinium chelate administration in the late subacute time period.

Penetrating vessels from the basilar artery and adjacent segments of the posterior cerebral arteries supply the brainstem. Infarcts involving the pons are most frequently small, unilateral, and sharply marginated at the midline. This location reflects the distribution of paramedian penetrating arteries, which consist of paired branches. Bilateral pontine infarcts do occur but are less common than unilateral infarcts. Lateral pontine infarction is extremely uncommon. The predominant finding on MRI in early subacute pontine infarction is vasogenic edema. Contrast enhancement is consistently seen in late subacute pontine infarction.

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Figure 6. Late subacute lacunar (basal ganglia) infarction. On adjacent T2-weighted fast spin echo sections (A and B), abnormal high signal intensity is noted in the globus pallidus and body of the caudate nucleus on the right. Enhancement of both lesions is seen on the corresponding postcontrast T1- weighted sections (C and D). The use of intravenous contrast assists in lesion recognition (conspicuity) and in dating lesions. Involvement of both the globus pallidus and caudate nucleus is not uncommon and points to involvement of the lenticulostriate arteries. These small perforating vessels arise from the superior aspect of the proximal middle cerebral artery (M1 segment) and supply the globus pallidus, putamen, and caudate nuclei.

  • Pontine lacunar infarction

The pons, or metencephalon, extends from the pontomedullary junction caudally to the pontomesencephalic junction rostrally. It is subdivided into the basis pontis ventrally and the pontine tegmentum dorsally by an arbitrary coronal line drawn through the two medial lemnisci [13].

Figure 7. Brainstem perforators. Gross anatomic specimens of the anterior surfaces of the upper medulla, pons, and midbrain after opacification of the major branches with micropulverized barium. (A) Upper medulla and pons. The vertebral arteries (V) of each side join to form the basilar artery (BA) (B) at the pontomedullary junction. Paramedian perforating branches (horizontal arrow) penetrate the brainstem immediately adjacent to the BA to supply the anteromedian arterial territory. Short circumflex arteries (vertical arrow) extend a short distance laterally before entering the stem to supply the anterolateral arterial territory. Long circumflex arteries (arrowheads) arise directly from the BA or from larger traversing branches, such as the anterior inferior cerebellar artery (AICA) (A), to supply the lateral arterial territory. Note that the AICA passes between fascicles of cranial nerve (CN) 6 (6) and then extends laterally to run along the anterior surface of CN 7 (7), loop over CN 7, nearly touch CN 5 (5), and then return toward the surface of the stem along the anterior surface of CN 8 (8). (B) Upper pons and midbrain. (Click to enlarge figure)

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Figure 8. Intrinsic arterial territories of the low pons. Shaded areas displayed clockwise from anterior to posterior: anteromedial (a), anterolateral (b), and lateral (c) pontine vascular territories. Numbered structures include pontocerebellar fibers (1), pontine nuclei (2), corticospinal tract (3), medial lemniscus (4), spinothalamic tract (5), lateral lemniscus (6), superior olivary nucleus (7), facial nucleus (CN 7) (8), spinal nucleus (9) and tract (9′) of the trigeminal system (receiving CN 5, 7, 9, and 10), inferior cerebellar peduncle (10), lateral vestibular nucleus (CN 8) (11), superior vestibular nucleus (CN 8) (12), medial vestibular nucleus (CN 8) (13), fibers of the facial nerve (CN 7) (14 and 14′), abducens nucleus (CN 6) (15), fibers of the abducens nucleus (CN 6) (15′), and medial longitudinal fasciculus (16). (Click to enlarge figure)

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Figure 9. Intrinsic arterial territories of the midpons. Shaded areas displayed clockwise from anterior to posterior: anteromedial (a), anterolateral (b), and lateral (c) pontine vascular territories. Numbered structures include pontocerebellar fibers (1), pontine nuclei (2), corticospinal tract (3), medial lemniscus (4), spinothalamic tract (5), lateral lemniscus (6), motor trigeminal nucleus (CN 5) (7), principal sensory trigeminal nucleus (CN 5) (8), mesencephalic trigeminal nucleus (CN 5) (9), fibers of the motor root of CN 5 (10), fibers of the sensory root of CN 5 (11), superior vestibular nucleus (CN 8) (12), superior cerebellar peduncle (13), and medial longitudinal fasciculus (14). (Click to enlarge figure)

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Figure 10. Intrinsic arterial territories of the upper pons. Shaded areas displayed clockwise from anterior to posterior: anteromedial (a), anterolateral (b), lateral (c), and posterior (d) pontine vascular territories. Numbered structures include pontocerebellar fibers (1), pontine nuclei (2), corticospinal tract (3), medial lemniscus (4), spinothalamic tract (5), lateral lemniscus (6), superior cerebellar peduncle (7), mesencephalic trigeminal nucleus (CN 5) (8), locus ceruleus (nucleus coeruleus) (9), and medial longitudinal fasciculus (10). (Click to enlarge figure)

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Figure 11. Vascularization of the basis pontis and pontine tegmentum. (Click to enlarge figure)

Anatomy of pontine structures

The arterial territories of the pons are considered in four zones: a large anteromedial, smaller anterolateral, large to extremely large lateral, and (in the rostral pons only) a small dorsal arterial zone [13]. From ventral to dorsal, the pons comprises the following:

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Figure 12. Intrinsic arterial territories of the pons (multiple levels). (Note that the diagram is oriented with ventral to the bottom). The usual external arterial supply to each zone is given as a list of vessels in the lower right corner. (Click to enlarge figure)

anteromedial pontine structures

The anteromedial pontine structures include the medial pontine nuclei and pontocerebellar fibers, medial portions of the corticospinal tracts intermixed with corticopontocerebellar and corticobulbar fibers, medial portions of the medial lemnisci, fibers of the facial nerve (CN 7), small medial wedges of the abducens nuclei (CN 6) and some emerging sixth nerve fascicles, the paramedian pontine reticular formation (PPRF; horizontal gaze center), and the MLF.

Anterolateral pontine structures

The anterolateral pontine structures include the lateral pontine nuclei and pontocerebellar fibers, lateral portions of the corticospinal tracts intermixed with corticopontocerebellar and corticobulbar fibers, sixth nerve fascicles (lower pons), and small midlateral portions of the medial lemnisci (variable). Depending on the specific caudorostral level along the axis of the pons, the anterolateral zone may terminate ventral to the medial lemnisci or extend into the medial lemnisci. It typically does not extend further dorsally into the pontine tegmentum. The anterolateral zones do not extend far enough laterally to involve the spinothalamic tracts [13].

Lateral pontine structures

The lateral pontine structures are comprised of two separate pontine regions (the upper and lower). In the large lateral zone of the low to midpons, lateral pontine infarctions include the lateral pontine nuclei and pontocerebellar fibers, rostral portions of the inferior cerebellar peduncles (low pons only), middle cerebellar peduncles (low and mid pons), lateral portions of the medial lemnisci and lateral spinothalamic tracts, lateral lemnisci, facial nuclei and fascicles, the trigeminal complex (including the spinal nuclei and tracts, motor nuclei and fascicles, and principal sensory nuclei and fascicles of CN 5), the vestibular complex (including the medial, superior, and lateral vestibular nuclei), and most of the abducens nuclei and their fascicles. At these levels, the fascicles of CN 7 arise from the laterally situated facial nuclei and course dorsomedially to the medial aspects of the abducens nuclei (CN 6). The facial fibers then recurve ventrolaterally around the rostral poles of the abducens nuclei to course ventrolaterally to their exits at the supraolivary fossettes. In the smaller lateral zone of the upper pons, lateral pontine structures include the lateral pontine nuclei and pontocerebellar fibers, lateral portions of the medial lemnisci and lateral spinothalamic tracts, lateral lemnisci, and a ventral portion of the superior cerebellar peduncle (uppermost pons only).

Dorsal pontine structures

The dorsal pontine structures are present in the upper pons only. No separate dorsal zones are found in the low to midpontine levels. Dorsal pontine structures include portions of the lateral lemnisci, portions of the superior cerebellar peduncles, the loci cerulei, and the mesencephalic nuclei of CN 5. The precise structures in each arterial territory vary from the low to high pons, so structures that extend along the length of the pons may exist in different vascular compartments at different pontine levels.

  • Blood supply to the pons

The blood supply to the pons derives primarily from the uppermost VAs, the BA, and the AICA and SCA branches of the BA:

Anteromedial pontine arterial zone

The anteromedial zone is supplied by anteromedial pontine perforators arising from the BA and entering (1) the foramen cecum at the midline pontomedullary junction inferiorly, (2) along the median sulcus of the pons in the middle, and (3) at the interpeduncular fossa superiorly.  [13]. These perforators follow different courses for the basis pontis and the pontine tegmentum. The perforators for the basis pontis pass directly posteriorly from the BA into the basis pontis. The perforators for the tegmentum arise in three major groups: (1) perforators for the inferior tegmentum pass from the BA into the foramen cecum at the pontomedullary junction and then ascend to supply the inferior pontine tegmentum; (2) perforators for the midtegmentum arise from the BA and pass directly posteriorly through the basis pontis to supply the midpontine tegmentum; and (3) perforators for the superior tegmentum arise from the interpeduncular branches of the BA, enter the stem via the interpeduncular fossa, and then descend to supply the superior pontine tegmentum.

Anterolateral pontine arterial zone

The anterolateral zone is supplied by anterolateral pontine perforators arising directly from the BA.

Lateral pontine arterial zone

The lateral zone is supplied by lateral pontine perforators that arise directly from the BA, from the AICA, or from the SCA. The inferior lateral pontine artery arises directly from the BA to supply the middle cerebellar peduncle. The superior lateral pontine artery arises directly from the BA to penetrate the lateral pons in the region of the entrance or exit zone of CN 5. Lateral pontine branches of the AICA and SCA may similarly irrigate the lateral zone.

Dorsal pontine arterial zone

Where present rostrally, the dorsal zone is supplied by posterior pontine perforators that arise from the SCA to supply the superior cerebellar peduncles.

External to the brainstem, the AICAs also supply the fibers of CN 6 in the prepontine cistern, the fibers of CN 7 and 8 in the cerebellopontine angles, and the petrous surfaces of the cerebellum. Internal auditory artery branches of the BA or AICA often supply the fibers of CN 7 and 8 within the porus acusticus. Occlusion of the internal auditory artery may cause ipsilateral hearing loss.

  • Function of the pontine structures

The functions of the pons are usually considered in terms of their intrinsic arterial territories.

Anteromedial pontine structure

The medial corticobulbar tracts contain motor fibers that cross in the upper pons to reach the bulbar nuclei to assist in movements of the eyes, face, pharynx, and tongue. Just lateral to these, the corticospinal tracts contain motor fibers for the upper extremities en route to the spinal cord. The corticopontocerebellar tracts receive fibers from the motor cortex and send fibers to the cerebellar nuclei via the middle cerebellar peduncles to assist with motor control. The medial portions of the medial lemnisci convey ascending fibers for vibration, proprioception, and deep sensation from the contralateral upper extremities. The fascicles of the facial nerve provide motor innervation to the ipsilateral face. The abducens nuclei and fascicles provide motor innervation to the lateral recti. The PPRF lies adjacent to the abducens nucleus and assists in horizontal gaze in the ipsilateral direction. At the lower pontine level, the MLF contain predominantly vestibulocervical spinal cord fibers to coordinate gaze with head motion, whereas at the upper pontine level, the MLF contain predominantly fibers that extend between CN nuclei 3 and 6 to coordinate horizontal gaze.

Anterolateral pontine structure

The lateral corticopontine nuclei connect extrapyramidal fibers from the cortex with the contralateral cerebellum to assist in motor control. Lateral portions of the corticospinal tracts contain predominantly motor fibers traveling to the contralateral lower extremity. Sixth nerve fascicles innervate the ipsilateral lateral rectus muscle to provide ipsilateral monocular abduction. Lateral portions of the medial lemnisci provide contralateral vibration and position sense, especially for the lower extremities.

Lateral pontine structure

The lateral pontine nuclei and pontocerebellar fibers make up a small portion of the lateral territory. The rostral portions of the inferior cerebellar peduncles in the lower pons convey inflow tracts to the cerebellum to assist in motor control. The middle cerebellar peduncles in the midpons carry corticopontine fibers from the pons to the cerebellum to assist in control of movement. Lateral portions of the medial lemnisci receive contralateral fibers concerned with joint position sense and vibratory sense from the contralateral upper and lower extremities. The spinothalamic tracts carry pain and temperature sensation from the contralateral body and extremities, excluding the face. The lateral lemnisci carry multisynaptic auditory input from the cochlear nuclei to the inferior colliculi. The facial nuclei and fascicles provide motor innervation to the ipsilateral facial muscles. The spinal nuclei and tracts of CN 5 carry pain and temperature sensation from the ipsilateral face. The motor nucleus of CN 5 provides innervation to the ipsilateral muscles of mastication (temporalis, masseter, medial and lateral pterygoid, tensor veli palatini, and tensor tympani muscles). The principal sensory nucleus of CN 5 receives ipsilateral light touch sensation from the face and subserves the corneal reflex. The pontine vestibular complex (medial, superior, and lateral vestibular nuclei) assists in maintaining equilibrium. The abducens nuclei and their fascicles innervate the lateral rectus for ipsilateral gaze. The facial fibers provide ipsilateral motor innervation to the facial muscles.

Dorsal pontine structure

The lateral lemnisci convey auditory fibers from the contralateral trapezoid body to the inferior colliculus. Portions of the superior cerebellar peduncles represent outflow tracts from the cerebellum to assist in motor control. The mesencephalic nuclei of CN 5 receive proprioceptive information from the muscles of mastication.

  • Infarction of the pons

Epidemiology of pontine infarcts

Isolated pontine infarcts make up 3% of all ischemic strokes and 12% of posterior circulation strokes [6]. Most pontine strokes result from hemodynamic effects of BA stenoses or occlusions or from atherosclerotic lesions that occlude the origins of small perforating arteries to the brainstem. Emboli account for fewer than 10% of ischemic strokes of the pons because emboli usually travel beyond the pons to lodge at the top of the BA. Dissections rarely cause ischemic pontine infarcts. Risk factors for pontine stroke include hypertension (73%), hypercholesterolemia (32%), diabetes mellitus (30%), and smoking (21%) [6]. Pontine infarctions affect men (53%) slightly more frequently than women (47%) [6].

Kumral and colleagues [6] divided pontine ischemic lesions into five possible syndromes: anteromedial pontine infarcts constitute 58% of pontine strokes, followed by the anterolateral pontine infarcts (17%), tegmental infarcts (10%), bilateral infarcts (11%), and multiple pontine infarcts (4%). Lateral pontine infarcts are uncommon (1 of 150 cases [0.7%]) [6]. These clinical groupings do not correspond directly with the vascular territories delineated by Duvernoy [13].

Anteromedial pontine infarcts

Anteromedial pontine infarcts cause dysfunction of the anteromedial structures injured: hemiplegia or hemiparesis from the corticospinal tracts; contralateral ataxia or pathologic laughter [22] from the corticopontine tracts; dysarthria, dysphagia, or contralateral facial palsy from the corticobulbar tracts; rare contralateral loss of proprioception from the medial lemnisci; ipsilateral facial palsy from the nuclei or fibers of CN 7; ipsilateral sixth nerve palsy from the fascicles of CN 6; and paresis of ipsilateral horizontal gaze from the PPRF or the nucleus of CN 6. Injury of the MLF leads to internuclear ophthalmoplegia (INO) with disconjugate lateral gaze. The ipsilateral eye is unable to adduct as it attempts to look to the contralateral side, whereas the contralateral eye abducts normally but shows horizontal nystagmus as it gazes to the contralateral side. The INO seen with pontine infarcts characteristically spares convergence. Pure motor strokes that involve the face, the arm, and the leg equally are the most common presentation of anteromedial pontine infarcts. By the somatotopic organization of motor fibers within the corticospinal tracts, however, extremely medial pontine infarcts may cause pure motor plegias of the arm and face out of proportion to leg weakness [23]. Because the corticospinal, corticopontine, and corticobulbar tracts lie together in the ventral pons, paresis or paraplegia may occur in conjunction with ataxia as part of the ataxic-hemiparesis syndrome or in conjunction with dysarthria as part of the clumsy-hand dysarthria syndrome. Pure sensory strokes and combined sensory-motor strokes are other possible presentations of the anteromedial syndrome. It must be noted that lacunar strokes of the internal capsule may cause the same clinical findings as pontine strokes, including pure motor stroke, ataxic hemiparesis, sensorimotor stroke, and clumsy-hand dysarthria, because the internal capsule is the one other site at which all these fibers converge [24].

Figure 13. Anteromedial pontine stroke. A 93-year-old-woman with dysarthria and right hemiparesis. Axial T2 (A) and diffusion-weighted (B) images. The narrow band of increased signal in the midpons reaching to the median raphe indicates an anteromedial medullary infarction. (Click to enlarge figure)

Table 1. Pontine stroke syndromes (Click to download in PDF format)

Anterolateral pontine infarcts

Anterolateral pontine infarcts cause dysfunction of the anterolateral structures injured, including plegia or paresis from the corticospinal tracts, ataxia or pathologic laughter from the corticopontine tracts, and vibration or proprioceptive loss from the medial lemnisci. Because the anterolateral zone of the pons contains the lateral portions of the same structures found in the anteromedial zone, the major clinical features of anterolateral pontine infarcts are similar to those of anteromedial pontine infarcts. Therefore, anterolateral infarcts may also present with pure motor stroke, ataxic hemiparesis, hypesthetic ataxic hemiparesis, clumsy-hand dysarthria, or sensorimotor stroke. Pontine infarctions may also involve the anteromedial and anterolateral zones in continuity. At times, however, subtle features may suggest that a pontine infarct is purely anterolateral. Because the lateral zones of the corticospinal tracts contain predominantly motor fibers to the lower extremities and the lateral zones of the medial lemnisci contain predominantly sensory fibers from the lower extremities, more severe weakness and loss of position sense in the lower extremities could theoretically signify anterolateral involvement. Further, because the anterolateral zones contain the spinothalamic tracts, loss of pain and temperature sensation from the contralateral trunk and extremities may also signify anterolateral zone infarction. Rare extension of the infarct into the tegmentum might present as conjugate gaze paralysis, vertigo, skew deviation, or INO.

Click to enlarge figure

Figure 14. Anterolateral pontine stroke. A 65-year-old-man with new right hemiparesis. Axial T2 (A) and diffusion-weighted (B) images. The paramedian band of increased signal in the midpons not reaching to the median raphe or the lateral pial surface indicates an anterolateral medullary infarction. (Click to enlarge figure)

Lateral pontine infarcts

Lateral pontine infarcts in the large lateral pontine zone of the low to midpons cause dysfunction of the lateral pontine structures injured, including ataxia from the inferior cerebellar peduncles, pontocerebellar fibers, and middle cerebellar peduncles; loss of pain and temperature sensation in the contralateral upper and lower extremities and trunk from the lateral spinothalamic tracts; tinnitus, reduced auditory acuity on either side, and abnormal sound lateralization from the lateral lemnisci [27–29]; ipsilateral motor deficits of the face from the facial nuclei and fascicles; loss of facial sensation, paresis of the ipsilateral muscles of mastication, and loss of the ipsilateral corneal reflex from the trigeminal complex; vertigo, nausea, and vomiting from the vestibular complex; and lateral rectus palsy from the abducens nuclei.

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Figure 15. Lateral pontine stroke. An 85-year-old-woman with slurred speech and weakness of the left face, arm, and leg. Axial fluid-attenuated inversion recovery (A) and diffusion-weighted (B) images. The posterolateral band of increased signal in the midpons with concurrent anterolateral cerebellar involvement indicates a lateral pontine infarction in association with an anterior inferior cerebellar artery infarction. (Click to enlarge figure)

Infarctions in the smaller lateral pontine zone of the rostral pons cause dysfunction of the lateral pontine structures injured, including ataxia from the pontocerebellar fibers, the middle cerebellar peduncles, and the superior cerebellar peduncles; loss of pain and temperature sensation in the contralateral upper and lower extremities and trunk from the lateral spinothalamic tracts; reduced auditory acuity and sound localization from the lateral lemniscus; and ipsilateral loss of jaw movement and facial sensation from the motor and sensory nuclei and fascicles of the trigeminal complex. These infarcts lie rostral to the nuclei and fascicles of CN 6, 7, and 8, so the patients do not display palsies of those cranial nerves.

Dorsolateral pontine infarcts

Dorsolateral pontine infarcts (at the same rostral level) cause dysfunction of the dorsolateral pontine structures, including reduced auditory acuity and sound localization from the lateral lemniscus or cochlear nucleus, ataxia from the superior cerebellar peduncles, theoretic parkinsonian symptoms from the loci cerulei, and decreased ipsilateral jaw jerk from the mesencephalic nuclei of CN 5. One small case series indicates that these lesions may manifest as sensorimotor or pure motor infarctions and often involve the leg more than the arm or face [30]. (See Table 1).

Three named but rare syndromes arise from infarcts in the (dorso)lateral arterial distribution (see Table 1):

1. Marie-Foix syndrome is a lateral pontine syndrome characterized by ipsilateral ataxia (from the middle cerebellar peduncle), contralateral hemiparesis (from the corticospinal tracts), and contralateral hypesthesia to pain and temperature (from the spinothalamic tract).

2. Foville syndrome is a dorsal caudal pontine infarct involving the PPRF, the nucleus and fascicles of CN 7, and the corticospinal tract; it is characterized by ipsilateral horizontal gaze paresis, ipsilateral peripheral facial palsy, and contralateral hemiparesis.

3. Raymond-Cestan-Chenais syndrome is a rostral dorsal pontine infarct characterized by ataxia (from the cerebellum), contralateral loss of facial and body sensation (from the medial lemniscus and spinothalamic tracts), and contralateral hemiparesis (from the corticospinal tracts).

Tegmental pontine infarcts

Tegemental pontine infarcts are characterized by predominant localization of the infarct to the dorsal (tegmental) portion of the pons. Clinically, tegmental infarcts exhibit prominent cranial nerve deficits and ataxia that are out of proportion to the motor findings. The overall picture may resemble other pontine syndromes but with more frequent diplopia, skew deviation of the eyes, abducens (CN 6) palsy, and vertigo.

Bilateral pontine infarcts

Bilateral pontine infarcts of the ventral pons disrupt the corticospinal, corticopontine, and corticobulbar fibers on both sides; the fascicles of the abducens nerve on both sides; the PPRF on both sides; and the reticular formation. These lesions typically present as acute or subacute onset of quadriplegia, aphonia, bilateral facial paralysis, and horizontal gaze paresis. Involvement of the reticular formation reduces consciousness initially, but consciousness returns later. Variable injury to the spinothalamic tracts may cause loss of pain and temperature sensation in the body and extremities (but not the face), or not. In severe cases, affected patients may be left with vertical gaze movements as their sole remaining motor function (“locked-in syndrome”). Overall outcome of vertebrobasilar steno-occlusion has traditionally been poor, with a mortality of 50% to 90% [31], although more recent data suggest the potential for good outcome in 71% of cases, residual severe disability in 23%, and death in 2.3% [32]. Those with locked-in syndrome, however, rarely have a meaningful recovery [33].

Hemipontine syndrome usually results from pontine hemorrhage but may be seen with ischemic pontine stroke secondary to occlusion of the BA or multiple BA branches [34]. The major manifestations include ipsilateral gaze paresis, ipsilateral facial weakness, contralateral hemiparesis, contralateral hemisensory loss of the face and extremities, contralateral ataxia, and dysarthria.

  • Brain stem lacunar infarction

In the elderly population with arteriosclerotic disease, lateral medullary infarction (Wallenberg’s syndrome) is not uncommonly encountered. This lesion is not clearly seen on CT. It is important for the radiologist to be familiar with the MRI appearance of this lesion and for the medulla to be included in the routine search pattern. Otherwise, a lateral medullary infarct may go unrecognized. Clinical presentation includes long-tract signs (contralateral loss of pain and temperature sensation, ipsilateral ataxia, and Horner’s syndrome) and involvement of cranial nerves V, VIII, IX, and X. Acute respiratory and cardiovascular complications can occur. In addition to the more common presentation resulting from thrombotic occlusion, lateral medullary infarction has also been reported after chiropractic neck manipulation. The latter occurs as a result of dissection of the vertebral artery near the atlantoaxial joint. The arteries supplying the lateral medulla typically arise from the distal vertebral artery but can originate from the PICA. Thus, lateral medullary infarction can accompany PICA infarction. Medial medullary infarction is less common than lateral medullary infarction. The clinical presentation of medial medullary infarction is that of contralateral hemiparesis, sparing the face.

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Figure 16. Lateral medullary infarction (early subacute). Abnormal hyperintensity is noted on the T2- weighted scan in the right lateral medulla (A). The T1-weighted scan (B) is grossly normal.


References

  1. Brown RD, Whisnant JP, Sicks JD, et al.. Stroke incidence, prevalence, and survival: secular trends in Rochester, Minnesota, through 1989. Stroke. 1996;27(3):373–380.

  2. Broderick J, Brott T, Kothari R, et al.. The Greater Cincinnati/Northern Kentucky Stroke Study: preliminary first-ever and total incidence rates of stroke among blacks. Stroke. 1998;29(2):415–421.

  3. Morris D, Schroeder E. Stroke epidemiology. Available at:http://www.uic.edu/com/ferne/pdf/strokeepi0501.

  4. Turney TM, Garraway WM, Whisnant JP. The natural history of hemispheric and brainstem infarction in Rochester, Minnesota. Stroke. 1984;15(5):790–794.

  5. Bogousslavsky J, Van Melle G, Regli F. The Lausanne Stroke Registry: analysis of 1,000 consecutive patients with first stroke. Stroke. 1988;19(9):1083–1092.

  6. Kumral E, Bayulkem G, Evyapan D. Clinical spectrum of pontine infarction. Clinical-MRI correlations. J Neurol. 2002;249(12):1659–1670.

  7. Kumral E, Bayulkem G, Akyol A, et al.. Mesencephalic and associated posterior circulation infarcts. Stroke. 2002;33(9):2224–2231.

  8. Martin PJ, Chang HM, Wityk R, et al.. Midbrain infarction: associations and aetiologies in the New England Medical Center Posterior Circulation Registry. J Neurol Neurosurg Psychiatry. 1998;64(3):392–395.

  9. Bogousslavsky J, Regli F, Maeder P, et al.. The etiology of posterior circulation infarcts: a prospective study using magnetic resonance imaging and magnetic resonance angiography. Neurology. 1993;43(8):1528–1533.

  10. Caplan LR, Wityk RJ, Glass TA, et al.. New England Medical Center Posterior Circulation registry. Ann Neurol. 2004;56(3):389–398.

  11. Kameda W, Kawanami T, Kurita K, et al.. Lateral and medial medullary infarction: a comparative analysis of 214 patients. Stroke. 2004;35(3):694–699.

  12. Bassetti C, Bogousslavsky J, Barth A, et al.. Isolated infarcts of the pons. Neurology. 1996;46(1):165–175.

  13. Duvernoy HM. The human brain stem and cerebellum surface, structure, vascularization and three-dimensional sectional anatomy with MRI. Wien (NY): Springer-Verlag; 1995;.

  14. Haines DE. Neuroanatomy: An atlas of structures, sections, and systems. 6th edition. Baltimore: Lippincott Williams & Wilkins; 2004;.

  15. Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 4th edition. Philadelphia: Lippincott Williams & Wilkins; 2001;.

  16. Carpenter MB. Core text of neuroanatomy. 4th edition. Baltimore: William & Wilkins; 1996;.

  17. Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain. 2003;126(Pt 8):1864–1872.

  18. Bogousslavsky J, Khurana R, Deruaz JP, et al.. Respiratory failure and unilateral caudal brainstem infarction. Ann Neurol. 1990;28(5):668–673.

  19. Brazis PW. Ocular motor abnormalities in Wallenberg’s lateral medullary syndrome. Mayo Clin Proc. 1992;67(4):365–368.

  20. Sacco RL, Freddo L, Bello JA, et al.. Wallenberg’s lateral medullary syndrome. Clinical-magnetic resonance imaging correlations. Arch Neurol. 1993;50(6):609–614.

  21. Mossuto-Agatiello L, Kniahynicki C. The hemimedullary syndrome: case report and review of the literature. J Neurol. 1990;237(3):208–212.

  22. Parvizi J, Anderson SW, Martin CO, et al.. Pathological laughter and crying: a link to the cerebellum. Brain. 2001;124(Pt 9):1708–1719.

  23. Kataoka S, Hori A, Shirakawa T, et al.. Paramedian pontine infarction. Neurological/topographical correlation. Stroke. 1997;28(4):809–815.

  24. Fisher CM. Lacunar strokes and infarcts: a review. Neurology. 1982;32(8):871–876.

  25. Shintani S, Tsuruoka S, Shiigai T. Pure sensory stroke caused by a pontine infarct. Clinical, radiological, and physiological features in four patients. Stroke. 1994;25(7):1512–1515.

  26. Shintani S, Tsuruoka S, Shiigai T. Pure sensory stroke caused by a cerebral hemorrhage: clinical-radiologic correlations in seven patients. AJNR Am J Neuroradiol. 2000;21(3):515–520.

  27. Furst M, Aharonson V, Levine RA, et al.. Sound lateralization and interaural discrimination. Effects of brainstem infarcts and multiple sclerosis lesions. Hear Res. 2000;143(1–2):29–42.

  28. Cho TH, Fischer C, Nighoghossian N, et al.. Auditory and electrophysiological patterns of a unilateral lesion of the lateral lemniscus. Audiol Neurootol. 2005;10(3):153–158.

  29. Sato K, Nitta E. A case of ipsilateral ageusia, sensorineural hearing loss and facial sensorimotor disturbance due to pontine lesion [in Japanese]. Rinsho Shinkeigaku. 2000;40(5):487–489.

  30. Kataoka S, Miaki M, Saiki M, et al.. Rostral lateral pontine infarction: neurological/topographical correlations. Neurology. 2003;61(1):114–117.

  31. Devuyst G, Bogousslavsky J, Meuli R, et al.. Stroke or transient ischemic attacks with basilar artery stenosis or occlusion: clinical patterns and outcome. Arch Neurol. 2002;59(4):567–573.

  32. Voetsch B, DeWitt LD, Pessin MS, et al.. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 2004;61(4):496–504.

  33. Mellado P, Sandoval P, Tevah J, et al.. [Intra-arterial thrombolysis in basilar artery thrombosis. Recovery of two patients with locked-in syndrome]. Rev Med Chil. 2004;132(3):357–360[in Spanish].

  34. Kushner MJ, Bressman SB. The clinical manifestations of pontine hemorrhage. Neurology. 1985;35(5):637–643.

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Ventriculitis
Jan 9th, 2013 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

January 9, 2013 — Ventriculitis is an uncommon CNS infection that has been described using a variety of terms including ependymitis, intraventricular abscess, ventricular empyema, and pyocephalus [1]. This variety of terms reflects various facets of the disease’s pathologic process. Because ventriculitis is a severe intracranial infection that can lead to serious sequelae and death, prompt diagnosis is necessary. However, the clinical features of ventriculitis are often obscure and nonspecific. MRI plays an important role as a first-line diagnostic tool in the diagnosis of ventriculitis [2].

Previously reported characteristic MRI findings of ventriculitis include intraventricular debris and pus, abnormal periventricular and subependymal signal intensity, and enhancement of the ventricular lining on conventional MRI sequences [3, 4]. In addition, a few reports have illustrated the usefulness of diffusion-weighted imaging for detecting intraventricular debris and pus [1, 3, 5]. We have encountered cases of ventriculitis in which the above MRI features were subtle on some MR pulse sequences but obvious on others. Thus, knowing which MRI sequences are useful for detecting the characteristic findings of ventriculitis is important for daily clinical practice.

Possible routes through which a pathogen might enter the intraventricular system include direct implantation secondary to trauma and postsurgical conditions, such as ventricular catheter placement; contiguous extension, such as the rupture of a brain abscess and extension into the ventricles; and hematogenous spread to the subependyma or the choroid plexus [2, 4, 7]. Back flow of CSF from the extraventricular spaces into the intraventricular space might be another possible route of infection leading to ventriculitis.

A blood clot in the ventricular system, caused by CSF backflow, is sometimes observed in cases of subarachnoid hemorrhage. This phenomenon is thought to arise from the alteration of pulsatile CSF flow dynamics by reduced compliance of the intracranial subarachnoid spaces as a result of the hemorrhage [8]. Other abnormalities of the subarachnoid space, including infection, might also contribute to changes in CSF flow. This concept might explain the observation that ventriculitis is often associated with meningitis.

  • MR imaging of ventriculitis

The most frequent sign of ventriculitis is intraventricular debris and pus. Abnormal periventricular intensities or enhancements are observed less frequently (85% on FLAIR images and 60% on contrast-enhanced T1-weighted images). Diffusion-weighted and FLAIR imaging concordantly show intraventricular debris and pus with an equally high detection rate. Thus, both of these sequences can be expected to contribute to the diagnosis of ventriculitis.

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Figure 1. A 68-year-old man with severe mastoiditis and acute petrositis. T2-weighted image shows areas of slight hypointensity relative to CSF in bilateral trigone of lateral ventricle. This finding is suggestive of intraventricular debris and pus. Slight ventricular wall abnormality is noted. B, FLAIR image shows hyperintense intraventricular lesions relative to CSF and hyperintensity along ventricular lining, suggesting ependymitis. C, Contrast-enhanced T1-weighted image shows abnormal curvilinear enhancement along the ventricular wall. Intraventricular debris and pus are slightly hyperintense relative to CSF. D, Diffusion-weighted image shows areas of conspicuous intraventricular and periventricular hyperintensity, indicating restricted water diffusion in those areas. E, Apparent diffusion coefficient (ADC) map shows areas of decreased ADC values in corresponding lesions on diffusion-weighted image (D).

The number of lesions detected in bilateral ventricles is higher on the diffusion-weighted images than on the FLAIR images. This discrepancy is likely caused by a difference in lesion conspicuity between the sequences. Although a quantitative evaluation was not performed, hyperintense intraventricular debris and pus were more conspicuous on the diffusion-weighted images than on the FLAIR images. In terms of visual inspection, diffusion-weighted imaging might provide better lesion contrast than FLAIR imaging for the detection of intraventricular debris and pus (Figs. 2A, 2B, 2C, 2D, 2E, 3A, 3B, 3C, 3D, 3E, 3F, and 3G).

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Figure 2. A 2-month-old boy with acute pyogenic meningitis. T2-weighted image shows slight dilatation of left occipital horn of lateral ventricle without findings of intraventricular and periventricular lesion. B, FLAIR image shows small area of slight hyperintensity in left occipital horn and slight hyperintensity along ventricular wall of left occipital horn. Leptomeningeal hyperintensity is also noted in left frontal region, suggesting meningitis. C, Contrast-enhanced T1-weighted image shows no significant enhancement of ventricular lining compared with meningeal enhancement in left frontal region, which is consistent with meningitis. D, Diffusion-weighted image reveals areas of intraventricular hyperintensity in bilateral occipital horn. Right intraventricular lesion is not detected on other sequence images. Periventricular abnormal signal intensity is indeterminate. E, Apparent diffusion coefficient (ADC) map shows decreased ADC values in areas corresponding to lesions on diffusion-weighted image (D).

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Figure 3. A 39-year-old man with AIDS and intracranial tuberculous infection. FLAIR image shows intraventricular lesions in left occipital horn of lateral ventricles with areas of hyperintensity along ventricular lining. Alteration of signal intensity in right occipital horn is minimal. Areas of hyperintensity suggesting infarction of bilateral basal ganglia and right frontal region are also seen. B, Contrast-enhanced T1-weighted image shows areas of slight hyperintensity relative to CSF in bilateral occipital horn. No periventricular enhancement is seen. C, Diffusion-weighted image reveals bilateral hyperintense intraventricular lesions with left predominance. D, FLAIR image 10 days after initial study shows newly developed cerebral lesion in left occipital region adjacent to left occipital horn in which intraventricular lesions have persisted. Areas of hyperintensity along ventricular wall are prominent. Dilated lateral ventricles and third ventricle are also newly seen. E, Contrast-enhanced T1-weighted image 10 days after initial study shows focal enhancement in left occipital region, suggesting cerebritis. No enhancement of ventricular wall is noted. F, Diffusion-weighted image 10 days after initial study shows areas of conspicuous focal hyperintensity in left occipital horn and along ventricular wall of bilateral occipital horn, which are different from other sequences in distribution. Hyperintensity in left occipital region suggests newly developed cerebritis. G, Diffusion-weighted image obtained at pons level 10 days after initial study shows hyperintensity in dependent portion of dilated fourth ventricle and in right cerebellopontine cistern, suggesting intraventricular debris and pus and meningitis, respectively.

Regarding the diffusion-weighted imaging findings, the lower mean ADC values of the hyperintense lesions might suggest the presence of material with restricted water diffusion in the ventricular space, consistent with previous descriptions of intraventricular debris and pus [1, 5] (Figs. 1A, 1B, 1C, 1D, and 1E). Intraventricular hemorrhage should be included in a differential diagnosis of intraventricular hyperintensity. However, clinical information would probably be helpful for distinguishing ventriculitis from intraventricular hemorrhage.

FLAIR imaging had the highest detectability rate for periventricular abnormalities, although this MRI finding is less frequent than intraventricular debris and pus. When symmetric abnormalities are present, the possibility of a periventricular inflammatory process should be considered. Areas of hyperintensity are frequently observed on FLAIR images of the periventricular white matter, particularly around the anterior and posterior horns of the ventricles. These areas of hyperintensity are called "caps and rims" and are considered to suggest age-related chronic ischemic changes in the white matter that are histologically characterized by myelin pallor, gliosis, and arteriosclerosis in the caps and subependymal gliosis and loss of the ependymal lining in the rims [6].

Choroid plexitis is thought to be another MRI finding associated with ventriculitis. Imaging findings for choroid plexitis have been well described and include a poorly defined margin of a swollen choroid plexus and contrast enhancement of the choroid plexus [9]. However, abnormal choroid plexus findings could not be identified with certainty on the diffusion-weighted and FLAIR images, possibly because the abnormal intensities produced by the intraventricular debris and pus is too bright, making it difficult to differentiate them from findings indicating choroid plexitis.

In conclusion, diffusion-weighted and FLAIR imaging may be valuable MRI sequences for detecting intraventricular debris and pus, suggestive of ventriculitis. Diffusion-weighted imaging may be particularly useful for recognizing intraventricular debris and pus because of the conspicuity of the lesions, drawing attention to the existence of ventriculitis. FLAIR imaging might be more valuable than contrast-enhanced T1-weighted imaging for depicting periventricular abnormalities, the second most common MRI feature of ventriculitis.


References

  1. Pezzullo JA, Tung GA, Mudigonda S, Rogg JM. Diffusion-weighted MR imaging of pyogenic ventriculitis. AJR2003; 180:71 -75

  2. Kanamalla US, Ibarra RA, Jinkins JR. Imaging of cranial meningitis and ventriculitis. Neuroimaging Clin N Am2000; 10:309 -331

  3. Fukui MB, Williams RL, Mudigonda S. CT and MR imaging features of pyogenic ventriculitis. Am J Neuroradiol2001; 22:1510 -1516

  4. Barloon TJ, Yuh WT, Knepper LE, Biller J, Ryals TJ, Sato Y. Cerebral ventriculitis: MR findings. J Comput Assist Tomogr 1990;14:272 -275

  5. Rana S, Albayram S, Lin DD, Yousem DM. Diffusion-weighted imaging and apparent diffusion coefficient maps in a case of intracerebral abscess with ventricular extension. Am J Neuroradiol2002; 23:109 -112

  6. Chimowitz MI, Estes ML, Furlan AJ, Awad IA. Further observations on the pathology of subcortical lesions identified on magnetic resonance imaging. Arch Neurol1992; 49:747 -752

  7. Lambo A, Nchimi A, Khamis J, Lenelle J, Francotte N. Primary intraventricular brain abscess. Neuroradiology2003; 45:908 -910

  8. de Marco G, Idy-Peretti I, Didon-Poncelet A, Baledent O, Onen F, Feugeas MC. Intracranial fluid dynamics in normal and hydrocephalic states: systems analysis with phase-contrast magnetic resonance imaging. J Comput Assist Tomogr 2004;28:247 -254

  9. Mathews VP, Smith RR. Choroid plexus infections: neuroimaging appearances of four cases. Am J Neuroradiol1992; 13:374 -378

  10. Takeshita M, Kawamata T, Izawa M, Hori T. Prodromal signs and clinical factors influencing outcome in patients with intraventricular rupture of purulent brain abscess. Neurosurgery2001; 48:310 -316

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Dysembryoplastic Neuroepithelial Tumor (DNT)
Dec 15th, 2012 by Administrator

The author: Professor Yasser Metwally

http://yassermetwally.com


INTRODUCTION

December 15, 2012 —  Dysembryoplastic Neuroepithelial Tumor (DNT) is a recently recognized, benign tumor associated with medically intractable, partial complex seizures. Mean age of onset of symptoms is nine years (range 1-19 years). All reported DNT’s have been supratentorial, most often involving the temporal lobe (approximately 2/3) followed in frequency by the frontal lobe (1/3). The tumors are primarily cortical in location, although they may extend to involve the subcortical white matter. On CT scans, DNT’s are well-defined, low-attenuation lesions which may be mistaken for cysts. The tumors tend to be low signal on T1- weighted MR images and high signal on T2-weighted images, i.e., similar to CSF, but on proton-density images, they are slightly higher in signal than CSF, allowing them to be differentiated from simple cysts. Less than 25% calcify or enhance. There is associated calvarial remodeling in approximately 1/3 of cases.

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Figure 1. Dysembryoplastic neuroepithelial tumor (Click to enlarge figure)

Differential diagnoses include ganglioglioma and low-grade astrocytoma. A ganglioglioma, however, is more likely to be located within the white matter. Calvarial remodeling, if present, is a helpful differentiating feature in that it would be unlikely for either a ganglioglioma or a low-grade astrocytoma to cause such changes.

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Figure 2. Dysembyroplastic neuroepithelial tumor. Coronal proton density-weighted image (A) and postcontrast (B) images demonstrate a peripherally based lesion (arrow) with trabeculated enhancement. Based solely on these images, it appears that the lesion is extra-axial because gray matter can be seen surrounding the lesion, especially in (A). However, it is not uncommon for an intra-axial neoplasm causing chronic epilepsy to appear extra-axial because it is situated within or replaces the cortex and has the appearance of being outside the cortex in some cross-sectional planes. Thin section imaging allowed visualization of the multicystic nature of this lesion on the enhanced image (B). (Click to enlarge figure)

The prognosis for patients with DNT is excellent. 70-81% of patients are seizure-free following surgery, and the tumor does not recur, even in cases where resection is considered incomplete.

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Figure 3. Photomicrograph (original magnification, x120; hematoxylineosin stain) of a dysembryoplastic neuroepithelial tumor shows neuronal elements surrounded by prominent vacuoles, which represent so-called floating neurons (arrows). (Click to enlarge figure)


References:

  1. Daumas-Duport C et al: Dysembryoplastic Neuroepithelial Tumor: A Surgically Curable Tumor of Young Patients With Intractable Partial Seizures. Neurosurgery 23:545-556, 1988.

  2. Kirkpatrick PJ, et al: Control of Temporal Lobe Epilepsy

  3. Following en bloc Resection of Low-grade Tumors. J. Neurosurg 78:19-25, 1993.

  4. Koeller KK, Dillon WP: Dysembryoplastic Neuroepithelial Tumors: MR Appearance. AJNR 13:1319-1325, Sept/Oct 1992.

  5. Morris HH, et al: Chronic Intractable Epilepsy as the Only Symptom of Primary Brain Tumor. Epilepsia 34:1038-1043, 1993.

  6. Taratuto AL, et al: Dysembryoplastic Neuroepithelial Tumor: Morphological Immunocytochemical, and Deoxyribonucleic Acid Analyses in a Pediatric Series. Neurosurgery 36:474-481, 1995.

  7. Toshiro K, et al: Radiologic Appearance of the Dysembryoplastic Neuroepithelial Tumor. Radiology 197:233-238, 1995.

  8. Vali AM, Clarke MA, Kelsey A: Dysembryoplastic Neuroepithelial Tumour as a Potentially Treatable Cause of Intractable Epilepsy in Children. Clinical Radiology 47:255-258, 1993.

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