Myoclonus in adult Huntington's disease

Two brothers with clinically definite adult Huntington's disease developed disabling myoclonus years after the first signs of the disease. Their electroencephalograms were consistent with a primary generalized epilipsy, although neither man had seizures. The myoclonus was controlled with valproic acid therapy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50341/1/410290217_ftp.pd

Dopamine D-1 and D-2 receptor antagonists potentiate analgesic and motor effects of morphine

To examine the role of dopamine receptor subtypes mediating analgesic and motor responses to opioids, rats were pretreated with either saline or a selective D-1 or D-2 dopamine receptor antagonist 10 min prior to morphine (12 mg/kg IP). Analgesic response latency was determined using the hot plate test (52.5[deg]C and 55[deg]C), and catalepsy was assessed using the abnormal posture test. Morphine increased analgesic response latency to 44.5 +/- 7.9% of the maximum possible response, but had no cataleptic effect in the abnormal posture test. Pretreatment with either the D-1 antagonist, SCH 23390 (50-100 [mu]g/kg), or the D-2 antagonist, eticlopride (20-150 [mu]g/kg), potently enhanced morphine analgesia as measured on the 52.5[deg]C hot plate. Peak analgesic responses to morphine increased to 100 +/- 0% and 91.9 +/- 7.5% of maximum with the highest doses of SCH 23390 and eticlopride, respectively. These treatments also produced catalepsy. Increasing the hot plate temperature to 55[deg]C reduced response latency in groups treated with either dopamine receptor antagonist plus morphine. This indicates that the animals were capable of responding at a shorter latency and demonstrates that motor impairment cannot account for potentiation of morphine analgesia by D-1 and D-2 antagonists at 52.5[deg]C. These results show that the relationship between dopamine and opioids with respect to analgesic and motor systems involves both dopamine receptor subtypes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28042/1/0000481.pd

Differential effects of chronic partial myelotomies on monoamine levels in cat spinal cord

The concentration of 5-hydroxytryptamine (5-HT), norepinephrine (NE) and dopamine (DA) were measured in samples of lumbar and cervical spinal cords from 6 cats with chronic (over 2 months) lesions of the thoracic spinal cord and from 7 unoperated cats. Lesions confined to the dorsal thoracic spinal cord significantly lowered lumbar concentrations of NE, but not 5-HT, compared with control lumbar or matched paired cervical samples. Both NE and 5-HT were significantly reduced by dorsal or ventral lesions that involved tissue ventral to the central canal. Only the largest lesion could be shown to reduce lumbar DA concentration.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26735/1/0000286.pd

Treatment for Vestibular Disorders: How Does Your Physical Therapist Treat Dizziness Related to Vestibular Problems?

Dizziness is very common, but it is never normal. Dizziness can make performing daily activities, work, and walking difficult. Many people get dizzy when they turn their head, which can cause problems with walking and makes people more likely to fall. Most of the time dizziness is not from a life-threatening disease. Often dizziness is because of a disorder of the vestibular (or inner ear balance) system. People can get vestibular disorders from infections in the ear, problems with the immune system, medications that harm the inner ear, and rarely from diabetes or stroke because of a lack of blood flow to the inner ear. Stress, poor sleep, migraines, overdoing some activities, and feeling sad can increase symptoms. New guidelines for the treatment of vestibular disorders were published in the April 2016 issue of the Journal of Neurologic Physical Therapy. The guideline describes which exercises are best to treat the dizziness and balance problems commonly seen with an inner ear disorder

Role of central epinephrine in regulation of anterior pituitary hormone secretion

Hypothalamic regulation of anterior pituitary hormones is thought to be mediated by the release of stimulatory and/or inhibitory peptides that are, in turn, regulated by catecholaminergic neurons. The recent development of selective epinephrine (EPI) synthesis inhibitors has made it possible to disrupt central EPI neurotransmission without affecting norepinephrine or dopamine. These compounds were used in the present investigation to assess the involvement of brain EPI systems in regulation of GH, LH, and prolactin (PRL) in male and ovariectomized female rats. Inhibition of central EPI synthesis (1) inhibited episodic and morphine-, but not clonidine-induced GH release, and (2) blocked the LH surge induced by estrogen and progesterone, but did not affect episodic LH release in hormonally untreated rats. Inhibition of peripheral (adrenal) EPI synthesis had no effect on these hormones. Results of these studies suggest an excitatory role for EPI in regulation of GH and LH secretion, mediated by stimulation of GH-releasing hormone and LHRH, respectively. EPI does not appear to have a major function in regulation of PRL secretion.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/23999/1/0000248.pd

Cocaine: evidence for supraspinal, dopamine-mediated, non-opiate analgesia

Cocaine (25 mg/kg i.p.) produces analgesia in the rat within 5 min and for a duration of 90 min as determined by the formalin test or for 30 min as determined by the hot plate test. Cocaine analgesia is unaffected by doses of naloxone that are sufficient to attenuate morphine analgesia in both tests. Chlorpromazine (3 mg/kg i.p.), SCH 23390 (100 [mu]g/kg i.p.; a D1 dopamine receptor antagonist), and eticlopride (75 [mu]g/kg i.p.; a D2 dopamine receptor antagonist) each attenuate cocaine analgesia in both tests at doses that alone do not affect performance in either test. Measurements of blood pressure and heart rate indicate that cocaine analgesia is not due to the activation of baroreceptor reflex afferents. We conclude that cocaine is a supraspinally acting, dopamine-mediated, non-opiate analgesic in the rat.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28057/1/0000496.pd

Vestibular Rehabilitation for Peripheral Vestibular Hypofunction: An Evidence-Based Clinical Practice Guideline: From the American Physical Therapy Association Neurology Section

Background: Uncompensated vestibular hypofunction results in postural instability, visual blurring with head movement, and subjective complaints of dizziness and/or imbalance. We sought to answer the question, \ Is vestibular exercise effective at enhancing recovery of function in people with peripheral (unilateral or bilateral) vestibular hypofunction?\ Methods: A systematic review of the literature was performed in 5 databases published after 1985 and 5 additional sources for relevant publications were searched. Article types included meta-analyses, systematic reviews, randomized controlled trials, cohort studies, case control series, and case series for human subjects, published in English. One hundred thirty-five articles were identified as relevant to this clinical practice guideline. Results/Discussion: Based on strong evidence and a preponderance of benefit over harm, clinicians should offer vestibular rehabilitation to persons with unilateral and bilateral vestibular hypofunction with impairments and functional limitations related to the vestibular deficit. Based on strong evidence and a preponderance of harm over benefit, clinicians should not include voluntary saccadic or smooth-pursuit eye movements in isolation (ie, without head movement) as specific exercises for gaze stability. Based on moderate evidence, clinicians may offer specific exercise techniques to target identified impairments or functional limitations. Based on moderate evidence and in consideration of patient preference, clinicians may provide supervised vestibular rehabilitation. Based on expert opinion extrapolated from the evidence, clinicians may prescribe a minimum of 3 times per day for the performance of gaze stability exercises as 1 component of a home exercise program. Based on expert opinion extrapolated from the evidence (range of supervised visits: 2-38 weeks, mean = 10 weeks), clinicians may consider providing adequate supervised vestibular rehabilitation sessions for the patient to understand the goals of the program and how to manage and progress themselves independently. As a general guide, persons without significant comorbidities that affect mobility and with acute or subacute unilateral vestibular hypofunction may need once a week supervised sessions for 2 to 3 weeks; persons with chronic unilateral vestibular hypofunction may need once a week sessions for 4 to 6 weeks; and persons with bilateral vestibular hypofunction may need once a week sessions for 8 to 12 weeks. In addition to supervised sessions, patients are provided a daily home exercise program. Disclaimer: These recommendations are intended as a guide for physical therapists and clinicians to optimize rehabilitation outcomes for persons with peripheral vestibular hypofunction undergoing vestibular rehabilitation

Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers

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