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PubMed1986

Movement deficits caused by hyperexcitable stretch reflexes in spastic humans.

Spastic patients were instructed to make accurate, rapid ankle dorsiflexion and plantarflexion movements over different distances to a target. Ankle position and surface electromyograms (EMGs) from tibialis anterior (TA) and soleus (SOL) muscles were recorded. In 3 of 8 spastic patients tested, dorsiflexion evoked velocity-dependent activation of the antagonist (SOL) muscle which impeded the movement to the extent that the limb unintentionally reversed movement direction. We propose that this activation is reflex in origin since it is tightly synchronized, has a large peak amplitude, occurs about 50 ms after the initiation of the movement, and is velocity dependent. One of the 3 patients who had reflex-induced antagonist activation in dorsiflexion also demonstrated sustained clonus during plantarflexion. This usually occurred only if the target had been overshot so that the return of the limb stretched the soleus muscle and triggered clonus. We conclude that in some patients, hyperactive stretch reflexes cause movement deficits.

Adult↗
PubMed1974

Spinal stroke.

Explore the source record for details and available documents.

Adult↗
PubMed1975

The tonic ambulatory foot response. A clinical and electromyographic study.

Three cases with "pyramidal" symptoms in which standing and/or walking evoked a tonic flexion of the toes and sole of the affected foot, have been studied from the clinical and electrophysiological standpoint. The phenomenon, for which the definition of tonic ambulatory foot respone (TAFR) is proposed, appeared to be triggered by cutaneous stimuli travelling along fibres lying in the range of nociceptive afferents, and to depend on a background of complex sensorimotor patterns of standing posture and/or stepping movements against resistance. The relationship of TAFR to other flexor foot responses described in the literature is discussed.

Cerebrovascular Disorders↗
PubMed2003

Cerebellar ataxia with bilateral vestibulopathy: description of a syndrome and its characteristic clinical sign.

We report four patients with the syndrome of cerebellar ataxia with bilateral vestibulopathy (CABV) and, using search coil oculography, we validate its characteristic clinical sign, namely impairment of the visually enhanced vestibulo-ocular reflex (VVOR) or doll's head reflex. In our four patients, CABV began in the sixth decade of life; they are still ambulant and self-caring 8-20 years after onset. The cause of CABV in our four patients is unknown. None has a family history of cerebellar or vestibular disease; spinocerebellar ataxia (SCA) 1, 2, 3, 6, 7 and Friedreich's ataxia were excluded by genetic testing. Three of the four have a sensory peripheral neuropathy but none has extrapyramidal or significant autonomic problems, and none has gluten sensitivity. We measured eye rotations in response to head-on-trunk head rotations and in response to head-and-trunk (en bloc) rotations. Horizontal smooth pursuit (SP), vestibulo-ocular reflex (VOR) and VVOR gains were measured in response to head rotations at 0.1, 0.3, 0.6 and 1.0 Hz. The optokinetic reflex (OKR) was tested by measuring optokinetic nystagmus slow phase velocity during constant 50 degrees /s rotation of the subject in light. The results showed that CABV patients had impairment of all three compensatory eye movement reflexes, the VOR, the OKR and SP. During VVOR testing, as the frequency of head rotation increased from 0.1 to 1.0 Hz, eye velocity failed to match head velocity, gaze velocity increased, and gaze position errors developed, which were corrected with bursts of saccades, the basis of the clinical sign of an impaired VVOR.

Adult↗
PubMed2003

Brief report: breast-fed one-week-olds demonstrate superior neurobehavioral organization.

OBJECTIVES: Following studies conducted during the immediate newborn stage, we investigated whether one-week-olds' neurobehavioral functioning was differentiated by feeding method. We also examined whether feeding-method effects differed among infants of adolescent mothers. METHOD: Participants were infants (N = 83) of breast-feeding (N = 41) and formula-feeding (N = 42) mothers. Approximately half of each group's participants had adolescent mothers and half were infants of adult mothers. Assessments on the Brazelton Neonatal Behavioral Assessment Scale (BNBAS) were conducted on the infants when they were 8.95 days of age. RESULTS: Breast-fed infants surpassed formula-fed infants on items of the orientation, motor, range of state, and state regulation dimensions of the BNBAS. Breast-fed infants also exhibited fewer abnormal reflexes, signs of depression, and withdrawal. Infants of adolescent mothers did not differ from those of adult mothers, regardless of feeding method. CONCLUSION: These data provide compelling evidence that breast-feeding is advantageous to neonates' neurobehavioral organization.

Adolescent↗
PubMed1988

Precasting work sheet--an assessment tool. A clinical report.

Physical therapists often use casting as an adjunct to traditional management of patients with brain injury. Casts generally are used on these patients for one of two reasons: 1) to increase range of motion with the use of serial casting or 2) to augment functional treatment with the use of inhibitive casting. This clinical report describes serial and inhibitive casts and introduces a precasting work sheet that promotes the selection of appropriate casting patients and necessary planning. The work sheet guides the therapist through an assessment of patient data relevant to casting, including passive range of motion, postural tone and abnormal reflexes, and voluntary movement. The precasting work sheet helps therapists gain expertise in casting by familiarizing them with the factors to consider before casting, encouraging them to set goals for casting, and helping them to determine whether the goals were met.

Brain Injuries↗
PubMed1985

Relationship of periodic movements in sleep (nocturnal myoclonus) and the Babinski sign.

To obtain a comprehensive clinical description of periodic movements in sleep, the first 11 videotaped movements of nine patients were studied. These leg movements were characterized by active dorsiflexion of the ankle (91%), dorsiflexion and fanning of the small toes (82%), and dorsiflexion of the great toe (72%). Partial flexion of the knee and hip occurred in 28%. Simultaneous dorsiflexion of the ankle and small toe was almost always the initial change, either preceding or occurring simultaneously with extension of the great toe. Knee and hip flexion almost always followed foot movements. Tonic and/or clonic movements, usually about the ankle, occurred in 75%; plantar flexion of the ankle occurred in 21% at the end of a leg movement. Periodic movements in sleep were thus characterized on detailed videographic analysis by movements similar to the Babinski response. Since both the normally occurring nocturnal Babinski response and periodic movements in sleep are also almost entirely NREM related, the author proposes that periodic movements in sleep are due to the NREM loss of supraspinal inhibitory influences on the pyramidal tract and that the characteristic foot and leg movements are Babinski-type responses secondary to this.

Adult↗
PubMed1991

HIV-1, macrophages, glial cells, and cytokines in AIDS nervous system disease.

Hallmarks of central nervous system (CNS) disease in AIDS patients are headaches, fever, subtle cognitive changes, abnormal reflexes, and ataxia. Dementia and severe sensory and motor dysfunction characterize more severe disease. Autoimmune-like peripheral neuropathies, cerebrovascular disease, and brain tumors are also observed. Histological changes include inflammation, astrocytosis, microglial nodule formation, and diffuse de- or dysmyelination. Focal demyelination can also be seen. It is clear that AIDS-associated neurological diseases are correlated with greater levels of HIV-1 antigen or genome in tissues. In AIDS dementia, macrophages and microglial cells of the CNS are the predominant cell types infected and producing HIV-1. However, manifestations of the disease make it unlikely that direct infection by HIV-1 is responsible. It seems more likely that the effects are mediated through secretion of viral proteins or viral induction of cytokines that bind to glial cells and neurons. HIV-1 induction of such cytokines as interleukin 1 (IL 1) and tumor necrosis factor-alpha (TNF alpha) may lead to an autocrine feedback loop involving further productive virus replication and induction of other cytokines such as interleukin 6 (IL 6) and granulocyte-macrophage colony-stimulating factor (GMCSF). Interleukin 1 and TNF alpha in combination with IL 6 and GMCSF could account for many clinical and histopathological findings in AIDS nervous system diseases. As HIV-1 infected patients produce elevated levels of IL 1, TNF alpha, and IL 6, it will be important to make a formal connection between the presence of these factors in the CNS, which are all products of activated macrophages, astroglia, and microglia, their in vivo induction directly by virus or indirectly by virus-induced intermediates, and the clinical and pathological conditions seen in the nervous system in this disease.

AIDS Dementia Complex↗
PubMed2000

Signs and symptoms of the myofascial pain syndrome: a national survey of pain management providers.

OBJECTIVE: The goal of this study was to assess clinical consensus regarding whether myofascial pain syndrome (MPS) is a legitimate and distinct diagnosis as well as the signs and symptoms characterizing MPS. DESIGN: A standardized mailed survey with return postage provided. SUBJECTS: A total of 1,663 American Pain Society members in medically related disciplines listed in the 1996/1997 directory. OUTCOME MEASURES: A standardized survey assessing clinical opinion regarding whether MPS is a legitimate diagnosis, whether MPS is a clinical entity distinct from fibromyalgia, and the signs and symptoms believed to be "essential to," "associated with," or "irrelevant to" to the diagnosis of MPS. RESULTS: Of the 403 surveys returned, 88.5% respondents reported that MPS was a legitimate diagnosis, with 81% describing MPS as distinct from fibromyalgia. The only signs and symptoms described as essential to the diagnosis of MPS by greater than 50% of the sample were regional location, presence of trigger points, and a normal neurologic examination. Regarding the signs and symptoms considered to be essential or associated with MPS, more than 80% of respondents agreed on regional location, trigger points, normal neurologic examination, reduced pain with local anesthetic or "spray and stretch," taut bands, tender points, palpable nodules, muscle ropiness, decreased range of motion, pain exacerbated by stress, and regional pain described as "dull," "achy," or "deep." Sensory or reflex abnormalities, scar tissue, and most test results were considered to be irrelevant to the diagnosis of MPS by a large proportion of the respondents. CONCLUSIONS: There was general agreement across specialties that MPS is a legitimate diagnosis distinct from fibromyalgia. There was a high level of agreement regarding the signs and symptoms essential or associated with a diagnosis of MPS. Differences across specialties are discussed. This survey provides a first step toward the development of consensus-based diagnostic criteria for MPS, which can then be validated empirically.

Data Collection↗
PubMed1997

Transient middle cerebral artery occlusion by intraluminal suture: II. Neurological deficits, and pixel-based correlation of histopathology with local blood flow and glucose utilization.

We conducted a pixel-based analysis of the acute hemodynamic and metabolic determinants of infarctive histopathology in a reproducible model of temporary (2-hour) middle cerebral artery occlusion (MCAO) produced in rats by an intraluminal suture. Three-dimensional averaged image data sets of local cerebral blood flow (LCBF) and glucose utilization (LCMRglc) acquired in the companion study (Belayev et al., 1997) either at the end of a 2-hour period of MCAO or after 1 hour of recirculation were comapped (using digitized atlas-templates) with data sets depicting the frequency of histological infarction in a matched animal group (n = 8) in which 2 hours of MCAO was followed by 3-day survival, sequential neuro behavioral examinations, and perfusion-fixation and paraffin-embedding of brains for light-microscopic analysis. All rats developed marked postural-reflex and forelimb-placing deficits at 60 minutes of MCAO, signifying high-grade ischemia. Tactile placing deficits persisted during the 72-hour observation period while visual placing and postural-reflex abnormalities variably improved. Comapping of LCBF and histopathology showed that in those pixels destined to undergo infarction, LCBF measured at 2 hours of MCAO showed a sharp distributional peak centered at 0.14 mL/g/min. In 70% of pixels destined to infarct, LCBF at 2 hours of MCAO was 0.24 mL/g/min or below, and in 89% LCBF was below 0.47 mL/g/min (the upper limits of the ischemic core and penumbra, respectively, as defined in the companion study [Belayev et al., 1997]). Local cerebral glucose utilization measured at approximately 1 hour after 2 hours of MCAO was distributed bimodally in the previously ischemic hemisphere. The major peak, at 22 mumol/100g/min, coincided exactly with the distribution peak of pixels destined to undergo infarction, while in pixels with a zero probability of infarction, LCMRglc was higher by 12 to 13 mumol/100g/min. These results indicate that local blood flow at 2 hours of MCAO is a robust predictor of eventual infarction. Pixels with ischemic-core levels of LCBF (0% to 20% of control) have a 96% probability of infarction, while the fate of the penumbra is more heterogeneous: below LCBF of 0.35 mL/g/min, the probability of infarction is 92%, while approximately 20% pixels in the upper-penumbral LCBF range (30% to 40% of control) escape infarction. Our data strongly support the view that the likelihood of infarction within the ischemic penumbra is highly influenced by very subtle differences in early perfusion.

Animals↗
PubMed1992

Uninhibited anal sphincter relaxation syndrome. A new syndrome with report of four cases.

I report a new syndrome, in four patients, all male. Patients ranged from 36 to 43 years of age. The main complaint was fecal urgency with occasional fecal soiling. Physical examination as well as pressure and EMG studies of anal sphincters and levator ani muscle were all normal. The only positive finding was an abnormal rectoinhibitory reflex. The external anal sphincter did not contract either reflexively or voluntarily on rectal distension, leaving the relaxing internal sphincter unprotected and uncontrolled. The patients could not oppose the urge to defecate if conditions are inopportune, with resulting urgency and occasional fecal soiling. The cause is unknown, but biofeedback effected improvement in all four cases.

Adult↗