The cerebellum
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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Studies of human TBI demonstrate that the cerebellum is sometimes affected even when the initial mechanical insult is directed to the cerebral cortex. Some of the components of TBI, including ataxia, postural instability, tremor, impairments in balance and fine motor skills, and even cognitive deficits, may be attributed in part to cerebellar damage. ⋯ In addition, we describe models that produce direct trauma to the cerebellum as well as those that reproduce specific components of TBI including axotomy, stab injury, in vitro stretch injury, and excitotoxicity. Overall, these models reveal robust characteristics of cerebellar damage including regionally specific Purkinje cell injury or loss, activation of glia in a distinct spatial pattern, and traumatic axonal injury. Further research is needed to better understand the mechanisms underlying the pathogenesis of cerebellar trauma, and the experimental models discussed here offer an important first step toward achieving that objective.
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The Pogo (pogo/pogo) mouse is a naturally occurring neurological mutant from a Korean wild-type mouse characterized by loss of balance and motor coordination due to dysfunction of the cerebellum. The Pogo mutation is believed to be an allele of P/Q-type calcium channel mutants such as tottering, leaner, and rolling mouse Nagoya. These mutants have been served as mouse models for a group of neurodegenerative diseases. ⋯ To address this issue, we first describe the discovery of Pogo mouse and its morphological and behavioral defects. Then, we focus on the abnormal expression of several molecules in the Pogo cerebellum, including tyrosine hydroxylase, glutamate, corticotrophin-releasing factor, and 5-hydroxytryptamine. Much of this review is concerned with the functional implications of these ectopic molecules in the Pogo cerebellum.
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Case Reports
Acute cerebellitis with cerebellar swelling successfully treated with standard dexamethasone treatment.
Although cerebellitis is common in childhood but cerebellitis with cerebellar swelling is rarely reported. Pulsed high dose methylprednisolone treatment is the choice of treatment for cases who have non-progressive symptoms. ⋯ Following treatment with standard dexamethasone dose, the clinical and radiological signs resolved in 1 week. We conclude that standard dexamethasone treatment should be used in mild cases of acute cerebellitis in order to avoid adverse reactions of pulsed high dose methylprednisolone treatment.
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Review
Human cerebellar responses to brush and heat stimuli in healthy and neuropathic pain subjects.
Though human pain imaging studies almost always demonstrate activation in the cerebellum, the role of the cerebellum in pain function is not well understood. Here we present results from two studies on the effects of noxious thermal heat and brush applied to the right side of the face in a group of healthy subjects (Group I) and a group of patients with neuropathic pain (Group II) who are more sensitive to both thermal and mechanical stimuli. Statistically significant activations and volumes of activations were defined in the cerebellum. ⋯ Further, innocuous brush stimuli in healthy subjects produced decreased cerebellar activation in lobules concerned with somatosensory processing. The data also suggest a dichotomy of innocuous stimuli/sensorimotor cerebellum activation versus noxious experience/cognitive/limbic cerebellum activation. These results lead us to propose that the cerebellum may modulate the emotional and cognitive experience that distinguishes the perception of pain from the appreciation of innocuous sensory stimulation.
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The neurogenic pulmonary edema is a rare clinical situation caused by an imbalance characterized by an excessive sympathetic outflow. It is observed mostly in young patients, is associated with brain or spinal cord haemorrhage, trauma, tumours or infections and is usually fatal. A case of neurogenic pulmonary edema in a 27-year-old woman is presented, caused by a cerebellar haemorrhage due to a vermian and paravermian arteriovenous malformation rupture. ⋯ Medical treatment with controlled ventilation, PEEP, diuretics and morphine reverted the pulmonary edema. After surgical treatment of the haemorrhage and cerebellar AVM the patient recovered to an almost normal social and professional life. The cerebellar lesion induced a temporary vermian sub lobule IX-b dysfunction that was responsible for the sympathetic storm that evoked the neurogenic pulmonary edema.