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PubMed1998

Ataxic hemiparesis: critical appraisal of a lacunar syndrome.

BACKGROUND AND PURPOSE: Ataxic hemiparesis is a well-recognized lacunar syndrome involving homolateral ataxia with accompanying corticospinal tract impairment. Despite 30 years of clinical experience there continues to be some doubt as to the defining clinical characteristics, precise neuroanatomic localization of the syndrome, and etiologic mechanisms. METHODS: We now present 45 new cases that have been analyzed for clinico-radiologic correlation and etiology. Also, all published cases from the English literature known to the authors are reviewed. RESULTS: We found that the clinical syndrome of ataxic hemiparesis accurately predicts a small deep infarction, generally in the pons or internal capsule. Sensory loss is highly associated with a capsular localization. We found that 47% of the cases were attributed to small-vessel disease, 11% to cardioembolism, and only 7% to artery-to-artery embolism (all in the basilar artery); 1 case was attributed to thrombocytosis, 1 to multiple sclerosis, and the rest either had negative or incomplete evaluation. Approximately two thirds of the infarctions occurred in patients with neuroimaging evidence of other ischemic brain lesions. CONCLUSIONS: Ataxic hemiparesis is a distinct clinical syndrome that accurately predicts a small deep infarction, most commonly in the pons or internal capsule. Only sensory loss accurately predicts a capsular localization. Etiology in nearly half of the cases can be attributed to small-vessel disease. Furthermore, ataxic hemiparesis appears to be a good marker for generalized asymptomatic cerebrovascular disease.

Adult↗
PubMed1983

Acquired capsular/striatal aphasia in childhood.

We studied a case of language loss caused by an acquired vascular lesion in the putamen, anterior limb of the internal capsule, and lateral aspect of the head of the caudate nucleus in a 7-year-old right-handed girl. Acute right-sided hemiplegia, mutism, oral apraxia, and disturbance in language comprehension but no dysarthria were present. During recovery, a nonfluent aphasia with anomia was evident. After six months, only mild hemiparesis and minor spelling difficulties persisted. We compared this patient with an 11-year-old right-handed girl with right-sided hemiparesis and dysarthria but no language loss following a lesion in the globus pallidus, a portion of the posterior limb of the internal capsule, and the body of the caudate. The presence of a language disturbance in the first but not the second patient was attributed to the difference in lesion location. The symptoms and lesions were similar to those in recent reports of adult patients. To our knowledge, this is the first report of these findings in a child with a left-hemisphere lesion.

Aphasia↗
PubMed2006

Changes in the kinematic structure and non-kinematic features of movements during skilled reaching after stroke: a Laban Movement Analysis in two case studies.

The purpose of this study was to adapt a universal language for human movement, Laban Movement Analysis (LMA), to capture the kinematic and non-kinematic aspects of movement in a reach-for-food task by subjects whose movements had been affected by stroke. Two control subjects, one stroke subject with internal capsule damage, and one subject with right posterior parietal stroke were video recorded while performing the reaching task. The movements of limb advancement, grasping the food, and limb withdrawal to place the food in the mouth, were notated using LMA. A scale, the Expressive Reaching Scale (ERS), was derived from the notation. All subjects completed the task; however, the stroke subjects displayed abnormalities in both the kinematic and non-kinematic aspects of movements during reaching with either limb. The most extensive impairments were in the contralateral-to-stroke limb and were most severe in the subject with internal capsule damage. The ERS rating scale may be a useful diagnosis and assessment tool.

Aged↗
PubMed1992

[Silent intracerebral lesions identified on magnetic resonance imaging in patients presenting with initial stroke--comparative studies of the affected hemisphere and the contralateral one].

Among patients who had undergone MRI examinations with a clinical suspicion of stroke, we selected 82 patients with initial cerebral infarction being located only in a unilateral cerebral hemisphere. Seventeen (21%) subjects had wedge-shaped lesions including cerebral cortex (the cortical type), 65 (79%) had them predominantly in white matter and/or territory of the deep perforators (the subcortical type). Fifty nine cases out of total 82 (72%:9 in the cortical type, 50 in the subcortical type) had the silent cerebral infarction in the contralateral hemisphere to the affected side found on the 1.5 tesla superconductive system T2 weighted magnetic resonance imaging. Among them, 57 had the contralateral small cortical and/or subcortical (white matter) infarction, the other 2 cases had the contralateral lacunar infarction in the basal ganglia-internal capsule area as the silent lesion. The incidence of the cortical type was high in cases without the silent cerebral infarction in the contralateral hemisphere. It might be suspected that the cortical type had tendency to present clinical symptoms caused by initial stroke without prior silent cerebral infarction. The author proposed that the cerebral embolism might play an important role in showing the sudden onset clinical symptoms of the cortical type. And the author also proposed that there might be a difference in the development of clinical symptoms between the silent cerebral infarction located in the basal ganglia-internal capsule area and the cortical-subcortical (white matter) area.

Aged↗
PubMed1997

MR of childhood metachromatic leukodystrophy.

PURPOSE: To investigate the MR findings of childhood metachromatic leukodystrophy (MLD). METHODS: Nine MR imaging studies in seven children (five girls and two boys, 10 to 32 months old) with MLD were evaluated retrospectively for the extent and progression of white matter abnormalities and the presence of contrast enhancement. RESULTS: All seven cases showed symmetric, confluent high signal intensity on T2-weighted images in the periventricular white matter and centrum semiovale. A posterior predominance of white matter abnormalities was noted in all cases. Although initially spared from demyelination in all cases, in one case, the subcortical U fibers were later involved in demyelination of follow-up MR studies. Other sites of involvement were the genu (n = 5) and splenium (n = 6) of the corpus callosum, the posterior limbs of the internal capsule (n = 5), the descending pyramidal tracts (n = 4), the claustrum (n = 4), and the cerebral white matter (n = 2); diffuse brain atrophy was seen in two cases. No enhancement of the lesion was seen on any of the five postcontrast examinations. A "tigroid" pattern, previously described in cases of Pelizaeus-Merzbacher disease, was noted in the centrum semiovale in six cases. CONCLUSION: In late-infantile MLD, demyelination is more prominent in the occipital region. In addition to demyelination of the periventricular white matter, common manifestations include a "tigroid" pattern and involvement of the corpus callosum, the internal capsule, and the corticospinal tract.

Brain↗
PubMed1995

Pathfinding by retinal ganglion cell axons: transplantation studies in genetically and surgically blind mice.

Optic axons show a highly stereotypical intracranial course to attain the visual centers of the brainstem. Here we examine the course followed by axons arising from embryonic retinae implanted in neonatal ocular retardation mutant mice in which there had been no prior innervation of the visual centers. Retinae placed on the ventrolateral brainstem adjacent to the normal site of the optic tract send axons dorsolaterally toward the ipsilateral superior colliculus, which they innervate along with a number of other subcortical visual centers. Somewhat unexpectedly, axons also course ventrally to cross at the level of the suprachiasmatic nucleus or, less frequently, caudal to the mammillary body to follow the route of the optic tract and innervate contralateral visual centers. Retinae implanted along the course of the internal capsule emit axons that follow projection fibers through the striatum to innervate the lateral geniculate nucleus and other optic nuclei. These grafts also appear to project to the lateral part of the ventrobasal nucleus of the thalamus. The results show that prior existence of an optic projection is not necessary for axons derived from ectopic retinae to attain visual nuclei, not only on the side of implantation but also on the contralateral side of the brain. The cues that these growing axons follow appear to be stable temporally. The fact that axons can also follow highly anomalous routes, such as through the internal capsule, to attain target nuclei in the brainstem suggests that the normal optic pathway is not an obligatory route for optic outgrowth.

Animals↗
PubMed2003

Diffusion-tensor MR imaging in children with developmental delay: preliminary findings.

PURPOSE: To determine whether diffusion-tensor magnetic resonance (MR) imaging can depict abnormalities in patients with a diagnosis of developmental delay but structurally normal brain MR imaging results. MATERIALS AND METHODS: Twenty pediatric patients who received a diagnosis of developmental delay underwent brain MR examinations, including diffusion-tensor MR imaging. The MR findings in these patients were compared with those in 10 age-matched neurodevelopmentally healthy children. Diffusion constant (Dav) and anisotropy were measured bilaterally in regions of interest in the centrum semiovale, corona radiata, internal capsule, corpus callosum, and subcortical white matter of the frontal and parieto-occipital lobes. By using a one-tailed Student t test in the positive direction for Dav and in the negative direction for anisotropy and P <.05 to indicate a significant difference, the Dav and anisotropy values for children with developmental delay were compared with those for children who were neurodevelopmentally healthy. RESULTS: The children with developmental delay had significant increases in Dav in all measured structures (P, <.001 to <.03). Significant decreases in anisotropy were detected in all white matter fiber tracts studied (P, <.001 to <.03) except the posterior limb of the internal capsule. CONCLUSION: In the children with developmental delay, diffusion-tensor MR imaging depicted decreases in anisotropy and increases in Dav in the white matter fiber tracts, which appeared to be normal at conventional MR imaging.

Anisotropy↗
PubMed2007

Repetitive activation of glutamatergic inputs evokes a long-lasting excitation in rat globus pallidus neurons in vitro.

External globus pallidus (GPe) neurons express abundant metabotropic glutamate receptor 1 (mGluR1) in their somata and dendrites and receive glutamatergic inputs mainly from the subthalamic nucleus. We investigated whether synaptically released glutamate could activate mGluR1s using whole cell and cell-attached recordings in rat brain slice preparations. Repetitive internal capsule stimulation evoked EPSPs followed by a slow depolarizing response (sDEPO) lasting 10-20 s. Bath application of both GABA(A) and GABA(B) receptor antagonists increased the amplitude of sDEPOs. A mixture of AMPA/kainate and N-methyl-d-aspartate receptor antagonists did not alter sDEPOs. The induction of sDEPOs was only partially mediated by mGluR1 because mGluR1 antagonists reduced but failed to completely block the responses. Voltage-clamp recordings revealed that slow inward currents sensitive to mGluR1 antagonist were larger at -60 than at -100 mV, whereas the currents insensitive to mGluR1 antagonist were larger at -100 than at -60 mV. In cell-attached recordings, repetitive internal capsule stimulation evoked long-lasting excitations in GPe neurons, which were also partially suppressed by mGluR1 antagonists. Application of a glutamate uptake inhibitor or an mGluR1 agonist significantly increased the spontaneous firing rate but decreased the excitations to repetitive stimulation. These results suggest that synaptically released glutamate can activate mGluR1, contributing to the induction of long-lasting excitation in GPe neurons and that background mGluR1 activation suppresses the slow mGluR1 responses. Thus mGluR1 may play important roles in the control of GPe neuronal activity.

Animals↗
PubMed2005

Spectroscopic evidence of cerebral axonopathy in patients with "pure" adrenomyeloneuropathy.

BACKGROUND: Adrenomyeloneuropathy (AMN) is the adult variant of X-linked adrenoleukodystrophy. The disease pathology is usually limited to spinal cord and peripheral nerves, and when this is the case, it is referred to as "pure" AMN. Histopathology shows cerebral involvement even in pure AMN; however, not much is known about the nature, extent, and clinical relevance of these findings. OBJECTIVE: To investigate brain involvement in AMN patients with normal MRI, employing multislice MR spectroscopic imaging. METHODS: Twelve men with pure AMN were compared with 19 age-matched healthy volunteers. Metabolite ratios (N-acetylaspartate [NAA]/choline [Cho], NAA/creatine [Cr], and Cho/Cr) were measured from seven brain regions. Global metabolite ratios were generated as an average of these seven regional ratios. The Expanded Disability Status Scale (EDSS) was used for neurologic evaluation. RESULTS: The patients with AMN showed reduced global NAA/Cho (AMN 1.40 +/- 0.16 vs controls 1.75 +/- 0.34; p = 0.003)) and global NAA/Cr (AMN 2.32 +/- 0.13 vs controls 2.62 +/- 0.43; p = 0.03). Regionally, NAA/Cho was lowered in the internal capsule (AMN 1.30 +/- 0.20 vs controls 1.69 +/- 0.37; p = 0.002) and in parieto-occipital white matter (AMN 1.45 +/- 0.19 vs controls 1.78 +/- 0.55; p = 0.04). NAA/Cr was lowered in parieto-occipital white matter (AMN 2.34 +/- 0.31 vs controls 2.83 +/- 0.71; p = 0.04). EDSS demonstrated an inverse association with global NAA/Cr (r = -0.65, p = 0.02) and NAA/Cr in centrum semiovale (r = -0.73, p = 0.006) and in parieto-occipital white matter (r = -0.64, p = 0.02). Cho/Cr was not significantly elevated. CONCLUSIONS: (1)H-MR spectroscopic imaging is able to detect biochemical abnormalities suggestive of axonal damage even in the brains of patients with pure adrenomyeloneuropathy. The axonopathy is most prominent in internal capsule and parieto-occipital white matter and may contribute to clinical disability.

Adrenoleukodystrophy↗
PubMed2006

Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy.

Brain water may increase in hepatic encephalopathy (HE). Diffusion tensor imaging was performed in patients with cirrhosis with or without HE to quantify the changes in brain water diffusivity and to correlate it with neuropsychological (NP) tests. Thirty-nine patients with cirrhosis, with minimal (MHE) or overt HE, were studied and compared to 18 controls. Mean diffusivity (MD) and fractional anisotropy (FA) were calculated in corpus callosum, internal capsule, deep gray matter nuclei, periventricular frontal, and occipital white matter regions in both cerebral hemispheres. The MD and FA values from different regions in different groups were compared using analysis of variance and Spearman's rank correlation test. In 10 patients with MHE, repeat studies were performed after 3 weeks of lactulose therapy to look for any change in MD, FA, and NP scores. Significantly increased MD was found with insignificant changes in FA in various regions of brain in patients with MHE or HE compared with controls, indicating an increase in interstitial water in the brain parenchyma without any microstructural changes. A significant correlation was found between MD values from corpus callosum, internal capsule, and NP test scores. After therapy, MD values decreased significantly and there was a corresponding improvement in NP test scores. Further analysis showed that MD values were different for different grades of minimal or overt HE. In conclusion, the increase in MD with no concomitant changes in FA in cirrhosis with minimal or early HE indicates the presence of reversible interstitial brain edema.

Adolescent↗
PubMed1999

Diffusion tensor MRI assesses corticospinal tract damage in ALS.

BACKGROUND: A number of neurophysiologic and neuroimaging techniques have been evaluated in the research setting to assess upper motor neuron (UMN) damage in ALS. Changes in tissue structure in the CNS modify the diffusional behavior of water molecules, which can be detected by diffusion tensor MRI. OBJECTIVES: To explore the hypothesis that degeneration of the motor fibers in ALS would be reflected by changes in the diffusion characteristics of the white matter fibers in the posterior limb of the internal capsule and that these changes could be detected by diffusion tensor MRI. METHODS: We studied 22 patients with El Escorial definite, probable, or possible ALS-11 with limb onset (mean age 54.5 +/- 10.7 years) and 11 with bulbar onset (mean age 49.6 +/- 11.7 years)-and compared them with 20 healthy, age-matched controls (mean age 46.0 +/- 12.6 years). We assessed central motor conduction time (CMCT), threshold to stimulation, and silent period using transcranial magnetic stimulation. Diffusion tensor MRI was performed using a 1.5-T GE Signa system (Milwaukee, WI) fitted with Advanced NMR hardware and software capable of producing echo planar MR images. Data were acquired from seven coronal slices centered to include the posterior limb of the internal capsule. Maps of the mean diffusivity, fractional anisotropy, and T2-weighted signal intensity were generated. RESULTS: There were no differences between the subject groups on measures of CMCT, threshold to stimulation, and silent period. However, the CMCT correlated with clinical measures of UMN involvement. We found a significant increase in the mean diffusivity and reduction in fractional anisotropy along the corticospinal tracts between the three subject groups, most marked in the bulbar-onset group. The fractional anisotropy correlated with measures of disease severity and UMN involvement, whereas the mean diffusivity correlated with disease duration. CONCLUSION: The results support the use of diffusion tensor MRI in detecting pathology of the corticospinal tracts in ALS.

Adult↗
PubMed2001

Chronic ischemia preferentially causes white matter injury in the neonatal rat brain.

Chronic ischemic brain injuries were studied in 7- and 14-day-old rat pups, which were subjected to bilateral carotid artery occlusion (BCAO) on postnatal day 1. BCAO preferentially injured white matter in the corpus callosum, subcortex and internal capsule areas while largely spared cortical neurons. White matter rarefaction in the corpus callosum was observed in 12 out of the 17 BCAO rat brains and significantly enlarged lateral ventricles were found in five out of seven P14 BCAO rat brains. These white matter changes were similar to injuries found in newborn infants with periventricular leukomalacia (PVL). White matter injuries in the 7-day-old BCAO rat brain were accompanied with increased activation of microglia/macrophages, as indicated by ED1 and OX42 positive immunostaining. Immature oligodendrocytes in the 7-day-old BCAO rat brain, as indicated by O4+/O1+ staining, were much fewer than in the sham-operated rat brain. Immunostaining for myelin basic protein (MBP) at the fimbria hippocampus and the internal capsule areas in the 7-day-old BACO rat brain was also much less than in the control rat brain. Consistent with the immunostaining data, MBP mRNA expression in the 7-day-old, but not in the 14-day-old, BCAO rat brain was significantly less than in the control rat brain. The overall results suggest that pre-oligodendrocytes and immature oligodendrocytes might be major targets for chronic ischemic insults and activated microglia/macrophages are possibly involved in the process of white matter injury.

Animals↗
PubMed2006

Panic and fear induced by deep brain stimulation.

BACKGROUND: Mood, cognitive, and behavioural changes have been reported with deep brain stimulation (DBS) in the thalamus, globus pallidus interna, and anterior limb of the internal capsule/nucleus accumbens region. OBJECTIVE: To investigate panic and fear resulting from DBS. METHODS: Intraoperative DBS in the region of the right and then left anterior limb of the internal capsule and nucleus accumbens region was undertaken to treat a 52 year old man with treatment refractory obsessive-compulsive disorder (OCD). Mood, anxiety, OCD, alertness, heart rate, and subjective feelings were recorded during intraoperative test stimulation and at follow up programming sessions. RESULTS: DBS at the distal (0) contact (cathode 0-, anode 2+, pulse width 210 ms, rate 135 Hz, at 6 volts) elicited a panic attack (only seen at the (0) contact). The patient felt flushed, hot, fearful, and described himself as having a "panic attack." His heart rate increased from 53 to 111. The effect (present with either device) was witnessed immediately after turning the device on, and abruptly ceased in the off condition CONCLUSIONS: DBS of the anterior limb of the internal capsule and nucleus accumbens region caused severe "panic." This response may result from activation of limbic and autonomic networks.

Anxiety↗
PubMed1992

[Cerebral single-photon emission-computed tomography. A semiquantitative analysis of vascular areas in patients with cerebrovascular pathology].

BACKGROUND: Brain SPECT perfusion studies in patients with cerebral stroke may be useful to evaluate distant perfusion abnormalities. METHODS: 99mTc-HMPAO brain SPECT studies were performed in 17 patients with ischemic lesions in the basal ganglia and/or internal capsule demonstrated by NMR. Regions of interest were adjusted in representative transverse slices to the vascular territories of the anterior, middle, posterior and communicating cerebral arteries. RESULTS: Patients with ischemic lesions in the right basal ganglia showed increased cerebral perfusion in the left middle artery territory (0.95 +/- 0.13 versus 0.80 +/- 0.06; p = 0.0365). Patients with ischemic lesions in the left basal ganglia showed increased perfusion in the right anterior artery territory (0.93 +/- 0.09 versus 0.82 +/- 0.09; p = 0.0464), in the left anterior artery territory (0.93 +/- 0.09 versus 0.83 +/- 0.14; p = 0.0464), in the left middle artery territory (0.92 +/- 0.09 versus 0.78 +/- 0.05; p = 0.0079) and in the left posterior artery territory (1.05 +/- 0.14 versus 0.90 +/- 0.09; p = 0.036). Patients with ischemic lesions in the right internal capsule showed increased perfusion in the right posterior artery territory (0.95 +/- 0.11 versus 1.10 +/- 0.18; p = 0.0431). CONCLUSIONS: These results show the presence of delayed luxury perfusion phenomena in regions distant from the ischemic site.

Aged↗
PubMed1989

[Cerebral blood flow in patients with thalamic hemorrhage (Part 2): Etiological analysis of decreased cerebral blood flow in acute stage].

In twenty-nine patients with thalamic hemorrhage, single photon emission CT (SPECT) and CT were performed in the acute stage. Measurement of cerebral blood flow (CBF) was performed by the 133-Xe inhalation method using SPECT (Tomomatic 64). CT findings such as hematoma volume, involvement of internal capsule, ventricular hematoma and topographical localization of hematoma were investigated. We studied etiological analysis of decreased CBF in the acute stage. CBF values in the group of large-volume hematoma (greater than or equal to 10 ml) decreased moderately on the hematoma side and mildly on the nonhematoma side. CBF values in the group of small-volume hematoma (less than 10 ml) decreased mildly on the hematoma side but didn't decrease on the nonhematoma side. CBF values of the former on the hematoma side decreased significantly compared with the latter. Linear correlation between hematoma volume and CBF was significant. As to topographical localization, CBF values of the group which involved medial thalamus decreased significantly compared with the other group. Factors of involvement of internal capsule and ventricular hematoma didn't affect CBF values. In conclusion, major factors which affected decreased CBF in the acute stage were hematoma volume and tomographical localization.

Acute Disease↗
PubMedDate not supplied

Specificity and sensitivity of betaAPP in head injury.

INTRODUCTION: Beta-amyloid precursor protein (betaAPP) expression has been found in traumatic brain injury, hypoxia, ischemia and infection which affect axonal transport. Although betaAPP is a sensitive marker for detecting axonal damage, it has become non-specific for a particular type of injury. The aim of this study was to identify a difference in the pattern, distribution and intensity of betaAPP expression in head injury compared to hypoxic/ischemic insults. MATERIALS AND METHODS: Thirteen primary head injury and 12 primary hypoxic/ischemic cases were selected. The anterior and posterior parts of corpus callosum, internal capsule (basal ganglia), middle cerebellar peduncles (cerebellum) and pons were examined and stained immunohistochemically for betaAPP antibody. A computerized system of image analysis was used to examine the intensity (strength of staining) and density (area fraction) of betaAPP. RESULTS: Significant differences were observed in the overall intensity and density of betaAPP expression (p < 0.05) and in all 5 brain regions in cases of head injury compared to the hypoxic/ischemic group (p < 0.05). Positive staining for betaAPP was found in all regions in all cases of head injury, however, 4 out of 12 cases of hypoxia/ischemia were positive for betaAPP. One case expressed positivity in all 5 regions, 2 cases exhibited positivity in the pons alone, with only 1 case exhibiting immunoreactivity in the posterior corpus callosum and internal capsule. Differences in the pattern of betaAPP expression identified a predominantly granular pattern with a dirty background seen in hypoxia/ischemia, while fusiform swellings, beaded and thick filaments with clear background were observed in head injury. CONCLUSION: There are differences in the pattern, distribution and intensity of betaAPP in head injury compared to hypoxia/ischemia. These could be due to pathophysiological differences. The results may be helpful in differentiating head injury from hypoxia in medicolegal cases.

Adolescent↗
PubMed1990

[Hematoma of the head of the caudate nucleus].

We studied five patients with cerebral hemorrhage limited to the head of the caudate nucleus. This rare localization represents 11% of central nuclei hemorrhages. This entity has various clinical expressions; some are similar to a subarachnoid hemorrhage, others show the same manifestations associated with hemiparesis and neuropsychological findings, while still in others, the neuropsychological syndrome with speech, behaviour or memory disturbances predominates. Recovery depends on the patient's previous clinical status and on the presence of associated lesions at the time of hemorrhage. Typical warning signs, like headache, are often absent in the elderly and debilitated. Meningismus is explained by the intraventricular extension of the hemorrhage. Motor deficit, usually moderate, is probably due to impairment of the anterior portion of the posterior arm of the internal capsule. Destruction of the head of the left caudate nucleus, which is part of the circuit causing "subcortical aphasias", is responsible for non specific speech disturbances, that are however remarkably rich in semantic paraphasias. These dysfunctions could be caused by a "cortical diaschisis" as suggested by SPECT analysis. Memory dysfunction as a result of caudate lesion is questioned. However confusion and behavioural disturbances, like preservations, transitory mutism and self neglect, seem characteristic. As shown by cerebral blood flow (CBF) studies, these disturbances might represent a frontal dysfunction caused by the interruption of the dorso-latero-prefrontal and orbito-frontal circuits. When the hemorrhage extends beyond the head of the caudate nucleus, behavioural changes occur due to the involvement of neighbouring structures such as the thalamus, internal capsule, temporal lobe and nucleus accumbens. Caudate hemorrhages occur mostly in the elderly, often with long-standing arterial hypertension causing lesions of the lenticulo-striate arteries. Severe stenosis or complete occlusion of the middle cerebral artery with a fragile anastomotic circuit or angiopathies in younger individuals (particularly Asiatics: moyamoya disease) are less frequent, but they should be considered and investigated by arteriography. Vascular malformations are a rare cause and a relationship with amyloid angiopathy can only be suspected.

Adult↗
PubMed1994

The pathological spectrum of diffuse axonal injury in blunt head trauma: assessment with axon and myelin strains.

Although diffuse axonal injury (DAI) has been described as a major form of primary damage to the brain in blunt head injury, there has been no systematic study of the pathological changes in different regions of the brain. In this study, 22 cases of DAI were comprehensively examined histologically in the following areas: corpus callosum, internal capsule, superior cerebellar peduncles, cerebral white matter, fornix, rostral brain stem and globus pallidus, with a total of 17 standard blocks in each case. Sections were stained for axons with Glees and Marsland and neurofilament immunostaining and myelin with luxol fast blue and myelin basic protein immunostaining, and axonal retraction balls and myelin globoids were counted. Neurofilament immunostaining was superior to Glees and Marsland in both the positivity rates and the actual scores. Small myelin globoids were identified by the myelin stains, probably as a form of myelin damage secondary to axonal disruption. Such acute myelin damage was previously undescribed. There was no significant difference in both positivity rates and the scores obtained for luxol fast blue and myelin basic protein. Of all the regions of the brain examined, the internal capsule, corpus callosum and superior cerebellar peduncles yielded the highest counts of axonal balls as well as the highest incidences. It is recommended that in cases of DAI, these three regions of the brain should be examined most profitably with neurofilament immunostaining supplemented with a myelin stain.

Adolescent↗