Hufnagel procedure reconverted by endovascular leaflet dislocation and extirpation

In 1914, Von Monakow described diaschisis, the recovery of lost cortical function in regions positionally distant from, but linked by neuronal tracts to, the primary site of cortical damage. Cerebellar diaschisis after cortical insult is detailed in the literature; however, cortical diaschisis after cerebellar insult remains a rarely reported occurrence. We describe a 36-year-old woman with rupture of a right-sided cerebellar arteriovenous malformation who developed such expected cerebellar signs as ataxia, dysmetria, and nystagmus. Days later, the patient developed profound impulsivity, disinhibition, and psychomotor agitation. Single photon emission computed tomography (SPECT) showed decreased perfusion of the bilateral frontal and temporal lobes, consistent with regional loss of neural activity. Eventual clinical improvement corresponded with reperfusion of those regions, identified on follow-up SPECT. This case documents cortical diaschisis following cerebellar insult and shows that diaschisis must be considered in patients with cerebral injury manifesting cortical deficits remote from the site of primary pathology.     

The alpha subunit of inhibin in adrenal cortical neoplasia

We analyzed 23 adrenal adenomas and 15 adrenal cortical carcinomas by immunolabeling for the alpha subunit of inhibin, and we then compared the results with the functional status of the neoplasms. We also studied 19 pheochromocytomas, 30 renal cell carcinomas, and 5 extra-adrenal paragangliomas, tumors posing differential diagnostic problems with adrenal cortical neoplasms. Immunolabeling was performed using automated immunohistochemical methods and an antibody directed against the alpha subunit. Tumors were semiquantitatively assessed for the number of positive cells. Immunopositivity was obtained in 18 (78%) of 23 adrenal cortical adenomas, 12 (80%) of 15 adrenal cortical carcinomas, 2 (11%) of 19 pheochromocytomas, 0 of 5 extra-adrenal paragangliomas, and 0 of 30 renal cell carcinomas. Immunoreactivity was strong in 7 (78%) of 9 adrenal cortical tumors from patients with Cushing's-related or virilizing symptoms. In contrast, only 4 (14%) of 29 tumors that were clinically nonfunctioning or associated with hyperaldosteronism demonstrated strong staining (P < .001). In clinically nonfunctioning tumors, there was a tendency for increased immunopositivity in tumors from patients with elevated levels of cortisol, androgen, or their precursors, with four of six tumors having at least moderate immunopositivity. Similar reactivity was present in only one of eight tumors from patients with normal laboratory values (P=.091). Moderate or strong immunopositivity was present in 9 (60%) of 15 adrenal cortical carcinomas, whereas of the pheochromocytomas, extra-adrenal paragangliomas, and renal cell carcinomas, only 1 (1.9%) of 54 showed moderate-to-strong reactivity. We conclude that moderate or strong immunoreactivity for the alpha subunit of inhibin occurs in adrenal cortical tumors from patients with Cushing's-related or virilizing symptoms. Immunolabeling for the inhibin alpha subunit is potentially useful in the differential diagnosis of neoplasms that include adrenal cortical carcinomas.     

Genome size and GC-percent in vertebrates as determined by flow cytometry: the triangular relationship

Cortical dysplasia is a broad category for an abnormal structure of the cerebrum due to a disorder of the normal developmental process for neocortex. We investigated the cortical dysplastic lesions which were surgically resected from 4 patients with intractable epilepsy. All cases showed a derangement of the cortical laminar structure and dysplastic changes in the neurons. In addition, 3 of them showed large round cells (balloon cells) in the deep cortex and subcortical white matter. Since each lesion showed slightly different features, we further examined the lesions immunohistochemically by using a panel of antibodies against cytoskeletal proteins to recognize and classify the cortical dysplastic lesions. An immunohistochemical study revealed marked abnormalities of the cytoskeletal structures of dysplastic neurons, bizarre glial cells and balloon cells. These cells showed an accumulation of either phosphorylated NF, MAP2 or GFAP in a distinct fashion. Ubiquitin immunoreactivity highlighted the extent of cortical dysplastic lesions. In a young patient, we also found the neuronal cytoplasmic lipofuscin deposition. It is thus considered that these diverse immunohistochemical appearances of cortical dysplasia may thus imply a different pathogenesis and they should therefore be classified based on the extent of histological abnormalities.     

Loss of tuberin from cerebral tissues with tuberous sclerosis and astrocytoma

We studied the expression of tuberin, the TSC2 gene product, in cerebra with or without tuberous sclerosis. Tuberin was abundant in the gray matter of normal cerebra, but was undetectable in the subependymal astrocytomas from 3 patients with tuberous sclerosis. In 1 patient, cortical tubers and normally appearing cortical tissue also showed a marked loss of tuberin. These results indicate the critical role of tuberin in the neuropathology of tuberous sclerosis.     

Correlation analysis of corticotectal interactions in the cat visual system

We have studied the temporal relationship between visual responses in various visual cortical areas [17, 18, postero medial lateral suprasylvian (PMLS), postero lateral lateral suprasylvian (PLLS), 21a]) and the superficial layers of the cat superior colliculus (SC). To this end, simultaneous recordings were performed in one or several visual cortical areas and the SC of anesthetized paralyzed cats, and visually evoked multiunit responses were subjected to correlation analysis. Significant correlations occurred in 117 (24%) of 489 cortex-SC pairs and were found for all cortical areas recorded. About half of the significant correlograms showed an oscillatory modulation. In these cases, oscillation frequencies covered a broad range, the majority being in the alpha- and beta-band. On average, significant center peaks in cross-correlograms had a modulation amplitude of 0.34. Our analysis revealed a considerable intertrial variability of correlation patterns with respect to both correlation strength and oscillation frequency. Furthermore, cortical areas differed in their corticotectal correlation patterns. The percentage of cells involved a corticotectal correlation, as well as the percentage of significantly modulated correlograms in such cases, was low for areas 17 and PMLS but high for areas 18 and PLLS. Analysis of the cortical layers involved in these interactions showed that consistent temporal relationships between cortical and collicular responses were not restricted to layer V. Our data demonstrate a close relationship between corticotectal interactions and intracortical or intracollicular synchronization. Trial-by-trial analysis from these sites revealed a clear covariance of corticotectal correlations with intracortical synchronization. The probability of observing corticotectal interactions increased with enhanced local cortical and collicular synchronization and, in particular, with interareal cortical correlations. Corticotectal correlation patterns resemble in many ways those described among areas of the visual cortex. However, the correlations observed are weaker than those between nearby cortical sites, exhibit usually broader peaks and for some cortical areas show consistent phase-shifts. Corticotectal correlations represent population phenomena that reflect both the local and global temporal organization of activity in the cortical and collicular network and do not arise from purely monosynaptic interactions. Our findings show that both striate and extrastriate inputs affect the superficial SC in a cooperative manner and, thus, do not support the view that responses in the superficial SC depend exclusively on input from the primary visual areas as implied by the concept of "two corticotectal systems." We conclude that the corticotectal projections convey temporal activation patterns with high reliability, thus allowing the SC evaluation of information encoded in the temporal relations between responses of spatially disseminated cortical neurons. As a consequence, information distributed across multiple cortical areas can affect the SC neurons in a coherent way.     

Correlation of near infrared spectroscopy cerebral blood flow estimations and microsphere quantitations in newborn piglets

We compared cerebral blood flow (CBF) estimated using transmission mode near infrared spectroscopy (NIRS) and a modification of the Fick principle with CBF quantitations by radioactive microspheres (MSs) in newborn piglets. Thirteen piglets were studied during steady state, ischemia, and during two reflow periods. NIRS and MS flows were not significantly different during any measurement period. NIRS flows were compared to total brain blood flows and to regional brain blood flows quantitated with MSs and correlated best with temporal cortical flows. Linear regression analysis of the NIRS flows plotted against MS-quantitated temporal cortical flows showed r = 0.71. Thus, CBFs obtained with NIRS were not significantly different from, showed the same directional changes, and correlated acceptably with flows quantitated by MSs.     

A case of cortical reflex positive-negative myoclonus--electrophysiological study

An 11-year-old girl who had the positive-negative myoclonus and the history of the generalized tonic clonic seizure was electrophysiologically studied. She had no siblings with either myoclonus or epilepsy, and her intellectual level was normal. She had no other neurological deficits including ataxia, pyramidal and extrapyramidal signs. Surface EMG showed a brief increase in the EMG activity followed by the silent period associated with positive and negative myoclonus during sustained wrist extension. Giant SEP and C reflex (38.6 ms) following electric stimulation of the median nerve at the wrist were obtained in the resting condition and the silent period (about 180 ms) following C reflex was obtained during voluntary contraction. Jerk-locked back averaging of the EEG time-locked to the onset of the myoclonic discharge recorded from the right biceps muscle showed a cortical spike at the left central region preceding the myoclonus onset by 12.6 ms. The latency of C reflex in this case was very short compared with that of previously reported cortical reflex myoclonus. The estimated cortical delay between the arrival of the somatosensory volley and the motor cortex discharge responsible for the C reflex was -1.0 ms and this value was shorter than that in patients with typical cortical reflex myoclonus (mean 3.7 +/- 1.1 ms). Conditioning stimuli (C) of the right median nerve at the wrist started to facilitate the amplitude of the motor evoked potential recorded from the right abductor pollicis brevis muscle after magnetic test stimuli (T) of the left motor cortex at 20 ms of the C-T interval. This C-T interval was shorter than that (24.6 +/- 1.6 ms) in patients with the typical cortical myoclonus. These electrophysiological findings suggested the shorter reflex pathway of the cortical reflex myoclonus in this case than in typical cortical reflex myoclonus. We speculated that the myoclonus was based upon the direct sensory projection from the thalamus to the motor cortex in this case.     

The distribution of neurons in the substantia nigra pars reticulata with input from the motor, premotor and prefrontal areas of the cerebral cortex in monkeys

We investigated the distribution of neurons in the substantia nigra pars reticulata (SNr) which received cortical input. The activities of single SNr neurons were studied extracellulary in awake monkeys. SNr neurons showed excitatory and/or inhibitory responses to cortical stimulation. These responses were considered to be mediated by the subthalamic nucleus and striatum, respectively. The neurons receiving inhibitory input from the motor, premotor and supplementary motor areas (Motor-related cortical areas) were located in the lateral part of the SNr, whereas those with input from the medial, dorsal and orbital areas of the prefrontal cortex (PFmdo) were frequently found in the rostro-medial part of this nucleus. SNr neurons with inhibitory input from the ventral periprincipal area (PSv) were mainly distributed in the intermedio-lateral portion, with some degree of overlap with input from other cortical areas. The distribution of the excitatory input was almost similar to that of inhibitory one, but the excitatory input from the PSv was much stronger than that from the PFmdo. Some SNr neurons receiving cortical input were proved to project to the thalamus. Our results support the existence of several parallel organization of the cortico-basal ganglia loop circuits [G.E. Alexander, M.R. DeLong, P.L. Strick, Parallel organization of functionally segregated circuits linking basal ganglia and cortex, Ann. Rev. Neurosci., 9, 1986, pp. 357-381.], but interaction between the loops can not be ignored.     

The effects of thrombocytopenia on the activated coagulation time

Cortical efferents grow from deep cortical layers to innervate numerous subcortical structures late in embryogenesis. The mechanisms that control their development are poorly understood. We co-cultured organotypic embryonic cortical explants with other tissues, maintaining a distance between them to avoid contact-mediated interactions. At embryonic day 15, when the cortical plate comprises only cells of the deep cortical layers, outgrowth from cultured cortex was stimulated by co-cultured subcortical structures, but not by additional cortex or liver. These data support the hypothesis that diffusible factors from subcortical structures, and not from the cortex itself, enhance cortical efferent growth.     

Variability and correlated noise in the discharge of neurons in motor and parietal areas of the primate cortex

We analyzed the magnitude and interneuronal correlation of the variability in the activity of single neurons that were recorded simultaneously using a multielectrode array in the primary motor cortex and parietal areas 2/5 in rhesus monkeys. The animals were trained to move their arms in one of eight directions as instructed by a visual target. The relationship between variability (SD) and mean of the discharge rate was described by a power function with a similar exponent ( approximately 0.57), regardless of the cortical area or the behavioral condition. We examined whether the deviation from mean activity between target onset and the end of the movement was correlated on a trial-by-trial basis with variability in activity during the hold period before target onset. In both cortical areas, for about a quarter of the neurons, the neuronal noise of these two periods was positively correlated, whereas significant negative correlations were seldom observed. Overall, neurons with higher signal correlation (i.e., similar directional pattern) showed higher noise correlation in both cortical areas. On the other hand, when the data were divided according to the distance between the electrode tips from which the neurons were recorded, a consistent relationship between the signal and noise correlations was found only for pairs of neurons recorded through the same electrode. These results suggest that nearby neurons with similar directional tuning carry primarily redundant messages, whereas neurons in separate cortical columns perform more independent processing.     

Emx1 and Emx2 show different patterns of expression during proliferation and differentiation of the developing cerebral cortex in the mouse

Insights into the complex structure of the forebrain and its regulation have recently come from the analysis of the expression of genes that are likely to be involved in regionalization of this structure. We cloned four new homeo box genes, Emx1, Emx2, Otx1 and Otx2, and showed that in day 10 mouse embryos their expression domains are continuous regions of the developing brain contained within each other in the sequence Emx1 < Emx2 < Otx1 < Otx2. Recently Otx1 has been found to be specifically expressed during neurogenesis of layer 5 and 6 in the developing cerebral cortex. In order to better understand the role of Emx1 and Emx2 in the maturation of the cortex we analysed by in situ hybridization their expression patterns in the developing mouse cerebral cortex, from embryonic day 12.5 to adulthood. We found that Emx2 is expressed exclusively in proliferating cells of the ventricular zone whereas Emx1 is expressed in both proliferating and differentiated neurons, throughout the cortical layers and during all the developmental stages examined. Therefore, Emx2 gene products might control some biological parameters of the proliferation of cortical neuroblasts or of the subsequent cell migration of postmitotic neurons, leaving the cortical germinal zone. Conversely, Emx1 expression, which is confined exclusively to the dorsal telencephalon, characterizes most cortical neurons during proliferation, differentiation, migration and postnatal development and maturation.     

Cortical gray matter volume deficits in schizophrenia: a replication

We sought to replicate an earlier finding of widespread deficit in cortical gray matter in schizophrenia by testing new samples of 22 schizophrenic patients and 27 controls between the ages of 21-46 years. Brain values for both patients and controls were standardized against age and head size norms derived from a larger control group (n = 73) spanning a wider age range (21-70). Compared to the new age-matched controls, the new schizophrenic sample showed a deficit in gray matter volume affecting the cortex as a whole and enlargement of the lateral and third ventricles. Thus, widespread cortical gray matter deficit is a replicable feature of the brain dysmorphology of schizophrenia in young to middle-aged men.     

Primary juxtacortical chondrosarcoma dedifferentiating after 20 years

We present the clinical, radiographic and pathological features of a juxtacortical chondrosarcoma which underwent dedifferentiation to an osteosarcoma in a 47-year-old woman. The tumour, abutting the femoral diaphysis, had initially presented 20 years earlier. Local excision was performed at presentation and again 10 years later, but the tumour recurred on each occasion. Serial radiographs showed cortical saucerisation evolving to cortical buttressing and mounding. After 20 years a dramatic radiographic change heralded tumour dedifferentiation.     

Visualization of the information flow through human oculomotor cortical regions by transcranial magnetic stimulation

We investigated the topography of human cortical activation during an antisaccade task by focal transcranial magnetic stimulation (TMS). We used a figure-eight shaped coil, with the stimulus intensity set just above the threshold for activation of the hand motor areas but weak enough not to elicit blinks. TMS was delivered at various time intervals (80, 100, and 120 ms) after target presentation over various sites on the scalp while the subjects performed the antisaccade task. It was possible to elicit a mild but significant delay in saccade onset over 1) the frontal regions (a region 2-4 cm anterior and 2-4 cm lateral to hand motor area) and 2) posterior parietal regions (6-8 cm posterior and 0-4 cm lateral to hand motor area) regardless of which hemisphere was stimulated. The frontal regions were assumed to correspond to a cortical region including the frontal eye fields (FEFs), whereas the parietal regions were assumed to represent a wide region that includes the posterior parietal cortices (PPCs). The regions inducing the delay shifted from the posterior parietal regions at an earlier interval (80 ms) to the frontal regions at a later interval (100 ms), which suggested an information flow from posterior to anterior cortical regions during the presaccadic period. At 120 ms, the effect of TMS over the frontal regions still persisted but was greatly diminished. Erroneous prosaccades to the presented target were elicited over a wide cortical region including the frontal and posterior parietal regions, which again showed a forward shift with time. However, the distribution of effective regions exhibited a clear contralateral predominance in terms of saccade direction. Our technique provides a useful method not only for detecting the topography of cortical regions active during saccadic eye movement, but also for constructing a physiological map to visualize the temporal evolution of functional activities in the relevant cortical regions.     

Effects of cyclosporine A and methotrexate on CD18 expression in recipients of rat cardiac allografts

We have electroporated Dictyostelium amoebae with fluorescent phalloidin in order to visualize the localization and behavior of F-actin filaments in living cells. Immediately after electroporation with phalloidin, cells became round and showed bright staining in the cortical region. Over time, the cortical staining disappeared and was replaced by a large aggregate of actin filaments. The aggregates were predominantly localized to the apical posterior of actively moving cells and in the middle of dividing cells or stationary AX4 cells. Mutants lacking myosin II or ABP-120 also formed actin aggregates; however, the rate of formation of aggregates was slower in myosin II mutant cells. In order to investigate this phenomenon further, we have used jasplakinolide, a membrane-permeable drug that also stabilizes F-actin filaments. Cells treated with jasplakinolide formed actin aggregates in a concentration-dependent manner. Drug treatment led to an increase in the proportion of actin associated with the cytoskeleton. Jasplakinolide-treated cells were still motile; however, their rate of movement was less than that of untreated cells. Cytochalasin B and nocodazole had inhibitory effects on aggregate formation, while azide blocked the process completely. We hypothesize that aggregates are formed from the cortical flow of F-actin filaments. These filaments would normally be depolymerized but are artificially stabilized by phalloidin or jasplakinolide binding. The localization of the aggregate is likely to be an indication of the direction of cortical flow.     

Mouse cortical neurones lacking APP show normal neurite outgrowth and survival responses in vitro

We have cultured neurones from the developing cortex of mice that have had the amyloid precursor protein gene deleted (APP-null). Neurones cultured for a period of 24 h show similar neurite outgrowth and survival responses to wild-type neurones. Similar neurite outgrowth responses were also seen when neurones from APP-null mice were treated with a neurotrophic peptide derived from the APP sequence and compared with wild-type neurones. Finally, cortical cultures derived from APP-null mice showed similar survival responses to the toxic amyloid-beta peptide.     

Cortical afferents of the perirhinal, postrhinal, and entorhinal cortices of the rat

We have divided the cortical regions surrounding the rat hippocampus into three cytoarchitectonically discrete cortical regions, the perirhinal, the postrhinal, and the entorhinal cortices. These regions appear to be homologous to the monkey perirhinal, parahippocampal, and entorhinal cortices, respectively. The origin of cortical afferents to these regions is well-documented in the monkey but less is known about them in the rat. The present study investigated the origins of cortical input to the rat perirhinal (areas 35 and 36) and postrhinal cortices and the lateral and medial subdivisions of the entorhinal cortex (LEA and MEA) by placing injections of retrograde tracers at several locations within each region. For each experiment, the total numbers of retrogradely labeled cells (and cell densities) were estimated for 34 cortical regions. We found that the complement of cortical inputs differs for each of the five regions. Area 35 receives its heaviest input from entorhinal, piriform, and insular areas. Area 36 receives its heaviest projections from other temporal cortical regions such as ventral temporal association cortex. Area 36 also receives substantial input from insular and entorhinal areas. Whereas area 36 receives similar magnitudes of input from cortices subserving all sensory modalities, the heaviest projections to the postrhinal cortex originate in visual associational cortex and visuospatial areas such as the posterior parietal cortex. The cortical projections to the LEA are heavier than to the MEA and differ in origin. The LEA is primarily innervated by the perirhinal, insular, piriform, and postrhinal cortices. The MEA is primarily innervated by the piriform and postrhinal cortices, but also receives minor projections from retrosplenial, posterior parietal, and visual association areas.     

Altered cortical blood flow in HIV-seropositive individuals with and without dementia: a single photon emission computed tomography study

OBJECTIVE: To quantitatively demonstrate the pattern of cerebral perfusion abnormalities in HIV-1-infected individuals described as 'patchiness' or inhomogeneity in previous qualitative emission tomographic imaging studies. DESIGN: We aimed to create a quantitative measure of inhomogeneity in HIV-infected individuals. High-frequency variance in cortical profiles is an indication of inhomogeneity in the distribution of radiotracer in the cerebral cortex. Therefore, the study analysis was designed to enable the estimation of variance frequencies in cortical profiles. METHODS: Regional cerebral blood flow was examined in nine mildly demented and 10 cognitively normal HIV-1-seropositive individuals and eight seronegative normal controls using single photon emission computed tomography with the radiotracer [I-123]-N-isopropyl-p-iodoamphetamine. Quantitative analysis was performed using circumferential profiles of cerebral cortical perfusion. Fourier transform power spectra of the profiles were examined as an index of patchiness in tracer distribution. RESULTS: Normal controls were characterized by strong middle frequency and weak high-frequency power. Both HIV-1-infected groups showed a significant power shift from middle to high frequencies. CONCLUSIONS: Increased high-frequency variations in both HIV-1-infected groups indicates diffuse cortical perfusion changes compared with normal controls. This study suggests that there are cerebral bloodflow abnormalities in HIV-1-infected individuals both with and without clinically severe dementia.     

Spike-wave complexes and fast components of cortically generated seizures. III. Synchronizing mechanisms

The intracortical and thalamocortical synchronization of spontaneously occurring or bicuculline-induced seizures, consisting of spike-wave (SW) or polyspike-wave (PSW) complexes at 2-3 Hz and fast runs at 10-15 Hz, was investigated in cats under ketamine-xylazine anesthesia. We used single and dual simultaneous intracellular recordings from cortical areas 5 and 7, and extracellular recordings of unit firing and field potentials from neocortical areas 5, 7, 17, 18, as well as related thalamic nuclei. The evolution of time delays between paroxysmal depolarizing events in single neurons or neuronal pools recorded from adjacent and distant sites was analyzed by using 1) sequential cross-correlations between field potentials, 2) averaged activities triggered by the spiky component of cortical SW/PSW complexes, and 3) time histograms between neuronal discharges. In all instances, the paroxysmal activities recorded from the dorsal thalamus lagged the onset of seizures in neocortex. The time lags between simultaneously impaled cortical neurons were significantly smaller during SW complexes than during the prior epochs of slow oscillation. During seizures, as during the slow oscillation, the intracortical synchrony was reduced with increased distance between different cortical sites. Dual intracellular recordings showed that, during the same seizure, time lags were not constant and, instead, reflected alternating precession of the recorded foci. After transection between areas 5 and 7, the intracortical synchrony was lost, but corticothalamocortical volleys could partially restore seizure synchrony. These data show that the neocortex leads the thalamus during SW/PSW seizures, that time lags between cortical foci are not static, and that thalamus may assist synchronization of SW/PSW seizures after disconnection of intracortical synaptic linkages.     

A meta-analysis of nausea and vomiting following maintenance of anaesthesia with propofol or inhalational agents

Methamphetamine (m-AMPH) administration injures both striatal dopaminergic terminals and certain nonmonoaminergic cortical neurons. Fluoro-Jade histochemistry was used to label cortical cells injured by m-AMPH in order to identify factors that contribute to the cortical cell body damage. Rats given four injections of m-AMPH (4 mg/kg) at 2-h intervals showed hyperthermia (mean = 40.0 +/- 0.10 degrees C) and increased behavioral activation relative to animals given saline (SAL). Three days later, m-AMPH-treated animals showed indices of injury to striatal DA terminals (depletion of tyrosine hydroxylase immunoreactivity) and parietal cortical cell bodies (appearance of Fluoro-Jade stained cells). Pretreatment with a dopamine (DA) D1, D2, or N-methyl-D-aspartate (NMDA) receptor antagonist, or administration of m-AMPH in a 4 degrees C environment, prevented or attenuated m-AMPH-induced hyperthermia, behavioral activation, and injury to striatal DA terminals and parietal cortical cell bodies. Animals pretreated with a DA transport inhibitor prior to m-AMPH showed hyperthermia, behavioral activation, and parietal cortical cell body injury, but they did not show striatal DA terminal injury. Pretreatment with a 5HT transport inhibitor failed to prevent m-AMPH-induced damage to striatal DA terminals or parietal cortical cell bodies. Animals given four injections of SAL in a 37 degrees C environment became hyperthermic, but showed no injury to striatal DA terminals or cortical cell bodies. The ability of the DA transport inhibitor to block m-AMPH-induced striatal DA damage, but not cortical injury, and the inability of hyperthermia alone to cause the cortical cell body injury suggests that m-AMPH-induced behavioral activation and hyperthermia may both be necessary for the subsequent parietal cortical cell body damage.