Contralateral cerebellar hypometabolism following cerebral insult: A positron emission tomographic study

Kushner, Michael; Alavi, Abass; Reivich, Martin; Dann, Robert; Burke, Anne; Robinson, G. D.

doi:10.1002/ana.410150505

Cited by 145 publications

(65 citation statements)

References 30 publications

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“…As reported in the current study, 6 h following a lateral F-P injury, the cerebral cortex and underly ing hippocampus ipsilateral to the site of insult ex hibited a marked decrease in LCMR g lc • This repli cates our previous work and agrees with several other studies exhibiting a dif fuse metabolic depression following cerebral isch emia (Kushner et al, 1984;Shiraishi et al, 1989), cortical freezing lesions (Pappius, 1981(Pappius, , 1982(Pappius, , 1988Papius and Wolfe, 1983;Colle et al, 1986), and sen sorimotor cortex ablations (Feeney et a1., 1985). Al though this metabolic diaschisis appears to be a rel atively common phenomenon following injury, the mechanisms behind its expression are not well un derstood.…”

Section: Hypometabolismsupporting

confidence: 92%

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Yoshino¹,

Hovda²,

Katayama³

et al. 1992

J Cereb Blood Flow Metab

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Summary: Immediately following fluid-percussion (F-P) brain injury, the hippocampus exhibits a marked increase in its local CMR g lc (LCMR g l c ; ILmol/lOO g/min) as deter mined using [14C]2-deoxY-D-glucose autoradiography. This injury-induced increase in metabolism is followed in 6 h by a subsequent decrease in LCMR g lc' These two postinjury metabolic states may be the result of ionic dis ruptions following trauma via stimulation of glutamate gated ion channels. To determine if endogenous gluta mate innervation to the CAl region of the hippocampus can provide an anatomical basis for this proposed mech anism, it was removed by kainic-acid-induced destruc tion of CA3, and the effect on CAl metabolism following concussive injury was studied. Five days before a lateral F-P injury (3.5-4.5 atm), kainic acid (0.5 ILg) or vehicle was stereotaxically injected into the left ventricle of 65 rats. Histological inspection indicated that kainic acid produced severe cell loss primarily in the CA3 region of the hippocampus ipsilateral to the injection. The meta bolic results indicated that immediately following injury, animals with an intact hippocampus exhibited an increase Following cerebral concussion in the rat, as pro duced using fluid-percussion (F-P) , the cerebral cortex and hippocampus exhibit pronounced changes in glucose metabolism. During the acute period, these regions exhibit a marked increase in this metabolism as determined by e 4 C]2-deoxY-D-

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Section: Hypometabolismsupporting

confidence: 92%

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Yoshino¹,

Hovda²,

Katayama³

et al. 1992

J Cereb Blood Flow Metab

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“…Because clinical symptoms and SPECT changes persisted after a follow-up period of 18 months, it is unlikely that the neurobehavioral syndrome of our patient was caused by metabolic changes in remote brain regions as described after cerebral infarction. 17 One cannot exclude the possibility that metabolic changes have determined the symptomatology and SPECT changes in 2 previously described patients, because SPECT findings were obtained respectively 16 and 20 days after stroke, 7 and metabolic changes in remote brain regions have been reported up to 3 months after stroke. 17 In conclusion, we report a case with a prominent residual loss of psychic self-activation after bilateral paramedian thalamic infarction documented during an 18-month follow-up period.…”

Section: Discussionmentioning

confidence: 99%

Loss of Psychic Self-Activation After Paramedian Bithalamic Infarction

Engelborghs

Mariën

Pickut

et al. 2000

Stroke

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Background and Purpose-Loss of psychic self-activation has been described after bilateral lesions to the globus pallidus, striatum, and white matter of the frontal lobes, but it is a very rare sign of bithalamic lesions. The exact functional-anatomic mechanism underlying loss of psychic self-activation following bithalamic lesions remains to be elucidated. Case Description-We present clinical, neuropsychological, structural, and functional neuroimaging data of an 18-month follow-up period of a man with prominent loss of psychic self-activation after coronary arteriography. Except for memory decline, accompanying symptoms remained restricted to the acute phase. The neurobehavioral syndrome consisted mainly of apathy, indifference, poor motivation, and flattened affect, and this remained unchanged during the entire follow-up period. MRI showed a bithalamic infarction involving the nucleus medialis thalami bilaterally. Single-photon emission CT revealed a severe relative hypoperfusion of both thalami, a relative hypoperfusion of both nuclei caudati, and a relative hypoperfusion mesiofrontally. Conclusions-Single-photon emission CT data support the hypothesis that the neurobehavioral manifestations after bithalamic paramedian infarction are caused by disruption of the striatal-ventral pallidal- We present a case with persistent apathy, unconcern, poor motivation, and flattened affect after recovery from acutephase symptomatology of a bilateral paramedian thalamic infarction. The so-called loss of psychic self-activation has been described after bilateral lesions to the globus pallidus, striatum, and white matter of the frontal lobes, 4 -6 but it is a very rare sign of bithalamic infarction. 7 Most cases with a loss of psychic self-activation after bithalamic injury have additional symptoms. Except for a memory decline, the accompanying symptoms in the present case remained restricted to the acute phase. Case ReportDuring a coronary arteriography, this 58-year-old righthanded patient suddenly developed a left hemiparesis and coma. The clinical neurological examination showed a comatose patient (Glasgow Coma Scale [GCS] E1V1M2) with equal pinpoint pupils and decerebrate rigidity. No eye movements could be elicited by the oculocephalic maneuver. Muscle tone of the left arm and leg were decreased. Tendon reflexes at the left arm and leg were increased. The left plantar response was extensor, whereas the right plantar response was flexor.For several hours, the patient exhibited fluctuating levels of consciousness, with GCS scores varying between 4 and 14. Muscle tone and strength rapidly normalized. Pupils and eye movements, including vertical gaze, were normal. Oculocephalic testing was unremarkable. Tendon reflexes were still brisker on the left side of the body than on the right side. The left plantar response remained extensor. Consciousness was fully recovered 3 days after stroke.The patient's behavior had dramatically changed. Instead of the active man he used to be, he had become an apathetic, passive, and indiffe...

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“…The proposal of RFD implies that measurable changes in some spared brain areas would be reflected in reduced neuronal activity and/or metabolism. Depressed metabolism has been reported in the Cb remote from areas of supratentorial tumors (Patronas et al, 1984) and strokes (Kurshner et al, 1984), but these were correlational observations. One way to test the RFD hypothesis is to determine whether manipulations influencing behavioral recovery after brain injury also influence measures of cerebral metabolism.…”

mentioning

confidence: 87%

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

et al. 1985

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Cerebral metabolic effects of locus coeruleus (LC) lesion or drugs affecting LC were investigated after unilateral injury of sensorimotor cortex in rats. Sensoriomotor cortex ablation produced a widespread depression of cerebral 14C-2-deoxyglucose utilization which was reversed by amphetamine (AMP, 2 mg/kg) and worsened by haloperidol (HAL, 0.4 mg/kg). Lesion of LC alone did not affect cerebral oxidative metabolism, measured by a stain for the enzyme alphaglycerophosphate dehydrogenase (a-GPDH). Lesion of LC prior to undercut laceration of motor cortex shortened time to onset of a-GPDH cortical paling. Treatment with AMP (2 mg/kg) blocked cortical paling ofthe enzyme stain at 4 days postinjury, an effect prevented by concomitant HAL (0.3 or 0.6 mg/kg). Apomorphine (1 mg/kg) did not block cortical paling. These data parallel effects of these drugs on recovery of function. The results suggest that a metabolic "remote functional depression" (RFD) is alleviated by catecholamine activation after cortical injury, whereas onset of RFD is accelerated by LC lesions and exacerbated by catecholamine blockade.The locus coeruleus (LC) may have an important role in neuronal development and plasticity (Felton, Hallman,

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Contralateral cerebellar hypometabolism following cerebral insult: A positron emission tomographic study

Cited by 145 publications

References 30 publications

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Loss of Psychic Self-Activation After Paramedian Bithalamic Infarction

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

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Contralateral cerebellar hypometabolism following cerebral insult: A positron emission tomographic study

Cited by 145 publications

References 30 publications

Hippocampal CA3Lesion Prevents Postconcussive Metabolic Dysfunction in CA1

Hippocampal CA3Lesion Prevents Postconcussive Metabolic Dysfunction in CA1

Loss of Psychic Self-Activation After Paramedian Bithalamic Infarction

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

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Product

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Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁