Increased Spontaneous Activity Produced in Monkeys by Brain Lesions

Richtee, Curt P.; Hines, Marion

doi:10.1093/brain/61.1.1

Cited by 82 publications

(28 citation statements)

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“…Classical literature using brain lesions identified the prefrontal cortical region as one that results in hyperactivity when damaged (Zubek and DeLorenzo, 1952), confirming earlier work in monkeys (Richter and Hines, 1938). Subsequent studies using lesions in rats identified the dorsal hippocampus as a specific region underlying persistent increases in exploratory behavior in rats (Kimble, 1963).…”

Section: Discussionsupporting

confidence: 79%

Metabolic changes over the course of aging in a mouse model of tau deposition

Joly‐Amado

Serraneau

Brownlow

et al. 2016

Neurobiology of Aging

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Weight loss and food intake disturbances that often precede cognitive decline and diagnosis have been extensively reported in Alzheimer’s disease patients. Previously, we observed that transgenic mice overexpressing tau seemed to eat more food, yet weigh less than non-transgenic littermates. Thus the present longitudinal study measured the time course of changes in metabolic state over the lifespan of the tau depositing Tg4510 mouse model of tau deposition. Although body weight was comparable to non-transgenic littermates at 2 months of age, Tg4510 mice weighed less at older ages. This was accompanied by the accumulation of tau pathology and by dramatically increased activity in all phases of the 24-hour cycle. Resting metabolic rate was also increased at 7 months of age. At 12 months near the end of the Tg4510 lifespan, there was a wasting phase, with a considerable decrease of resting metabolic rate, although hyperactivity was maintained. These diverse changes in metabolism in a mouse model of tau deposition are discussed in the context of known changes in energy metabolism in Alzheimer’s disease.

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Section: Discussionsupporting

confidence: 79%

Metabolic changes over the course of aging in a mouse model of tau deposition

Joly‐Amado

Serraneau

Brownlow

et al. 2016

Neurobiology of Aging

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“…In tense diffuse gliosis to the right of the peduncle was likewise found. Hyperkinesia as a conse quence of damage to the caudate nucleus has been demonstrated experimentally in various animals (Richter and Hines, 1938;Met tier and Mettler, 1942;Klosovskii and Valzhina, 1956;Davis, 1958;Whittier and Orr, 1962). In the last and in the 6th case the hyperkinesia syn drome was likewise caused by impairment of the caudate loop, limbic region of the cortical areas 6 and 8 and damage of some connections with the deep formations of the central grey nuclei, that induced the parkinsonian-like movements.…”

Section: Commentsmentioning

confidence: 96%

Logorrhea Syndrome with Hyperkinesia

Arseni¹,

Dănăilă²

1977

Eur Neurol

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“…At home, the patient's wife related that he had become bellicose and irritable and 'aged' considerably in the following months. Experimental bilateral damage in caudate nucleus of experimental animals usually produces hyperactivity (Richter and Hines, 1938;Mettler and Mettler, 1942) but sometimes produces a transitory state not too unlike akinetic mutism. For example, Gybels, Meulders, Callens, and Colle (1967) created bilateral electrolytic lesions in cats limited to the head of the caudate nucleus and for the next five days 'the animals were catatonic and abnormal positions could be imposed on them for several minutes'.…”

Section: Discussionmentioning

confidence: 99%

Akinetic mutism and bilateral anterior cerebral artery occlusion

Freemon

1971

Journal of Neurology, Neurosurgery & Psychiatry

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A 68 year old retired depressed white male was admitted to the surgical service because of a self-inflicted minor gunshot wound to the chest. The only significant past history was a myocardial infarction 13 years previously. After successful treatment of his chest wound the patient was transferred to the psychiatric service because of continued suicidal thoughts and statements. One morning a week later he awoke feeling unusually 'groggy' as he told his room-mate. On his way to the bathroom the patient fell and could not arise. When he was examined his eyes were open but he could not speak or follow commands. The doll's head manoeuvre showed extraocular movements to be full. Pupils were equal and reactive to light. Gag reflex was present as were corneal reflexes. A slight plastic rigidity was present in all limbs. The only move-.r K.1 ment elicitable was a slight withdrawal of each limb to deep pain stimulation. However, if the patient's arm was held over his face and allowed to drop, it usually fell in such a way as to miss his face. Tendon reflexes were bilaterally symmetrical and hyperactive, particularly in the lower extremities with sustained clonus at both ankles. Bilateral Babinski signs were present, as were snout and grasp reflexes. The patient would look at the examiner and would follow him with his eyes. Several attempts to communicate with the patient using eye movements or eye blinks as signals were entirely unsuccessful. Within an hour after the insult, an electroencephalogram was performed which showed low voltage 2-2i Hz generalized activity. A lumbar puncture showed an opening pressure of 140 mm CSF and a closing pressure of 120 mm CSF; glucose was 77 mg and protein 45 mg/100 ml. There were no cells in the CSF and there was no xanthochromia. The next morning the patient had lost his superficial appearance of alertness. His eyes were closed and his musculature was flaccid unless he was stimulated at which time he became rigidly opisthotonic with extension of legs and arms, with flexion at the wrists. He had CheyneStokes respiration with an apnoeic period of 20 seconds. At this time the pupils remained equal and reactive, extraocular movements were intact as estimated by the doll's head manoeuvre, and caloric examination showed conjugate tonic deviation of the eyes toward the side of the cold water. The patient died 10 days later.NEUROPATHOLOGICAL FINDINGS External examination revealed bilateral softening from the frontal pole to the inferior occipital region with slight clouding and thickening of the overlying meninges. Coronal sections showed severe infarction on the left, involving the entire frontoparietal and temporal cortex extending through subcortical white matter to the basal ganglia, including the head of the caudate nucleus but sparing the thalamus.

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Increased Spontaneous Activity Produced in Monkeys by Brain Lesions

Cited by 82 publications

References 0 publications

Metabolic changes over the course of aging in a mouse model of tau deposition

Metabolic changes over the course of aging in a mouse model of tau deposition

Logorrhea Syndrome with Hyperkinesia

Akinetic mutism and bilateral anterior cerebral artery occlusion

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