The Experts below are selected from a list of 174 Experts worldwide ranked by ideXlab platform

Mostafa M Elhilali - One of the best experts on this subject based on the ideXlab platform.

  • urinary bladder hyperreflexia a rat animal model
    Neurourology and Urodynamics, 2003
    Co-Authors: Hassa Shake, Mohammed Sherif Mourad, Mohammed Hatem Elbialy, Mostafa M Elhilali
    Abstract:

    In this work, we are presenting a rat animal model for bladder hyperreflexia after suprasacral Spinal cord transection. Our aim was to standardize an animal model that can be useful in studying this condition. After standardizing the animal model in a pilot study, 26 female Sprague–Dawley rats were subjected to Spinal cord transection at the level of T10 vertebra. Four animals were subjected to cystometrogram (CMG) 24 hr after Spinalization and six rats 3 weeks post-Spinalization. These CMGs were compared to that of six normal controls. The detailed description of the model presented in this manuscript, is the final result after several modifications. All the animals consistently developed hyperreflexia after an initial period of Spinal Shock phase. Expressed volume of urine continued to decrease until it reached a plateau after peaking at 1-week post-Spinalization. The attrition rate reached 27.3% after several improvements in the animal model and was mostly from self-inflicted injuries. Post-operative complications included hypothermia, decubitus ulcers, hematuria, urinary tract infection in addition to the unexplained death of two animals. In conclusion, we believe that this animal model closely resembles the clinical condition of hyperreflexia and follows similar course. The relative low cost of this animal model and the easy maintenance makes it a valuable tool to study such a condition. Neurourol. Urodynam. 22:693–698, 2003. © 2003 Wiley-Liss, Inc.

  • effect of early bladder stimulation on Spinal Shock experimental approach
    Urology, 1992
    Co-Authors: Mostafa M Elhilali, Magdy M Hassouna, Mohamad Sawan, F Duval, R Latt
    Abstract:

    The period of Spinal Shock which frequently follows Spinal cord injury is associated with bladder areflexia and urinary retention. We studied the effect of early bladder electric stimulation on detrusor activity during the Spinal Shock phase in the dog. The animals had a Spinal cord section at T10 vertebra, and their bladder management was assigned to one of the three following groups: intermittent catheterization, indwelling catheterization, and electric bladder stimulation. The parameters for evaluating each treatment included: blood chemistry, and radiographic and urodynamic tests. The most important finding was the early return of detrusor activity in the group of animals treated by early electric stimulation of the bladder.

John F. Ditunno - One of the best experts on this subject based on the ideXlab platform.

  • Spinal Shock revisited: a four-phase model
    Spinal Cord, 2004
    Co-Authors: John F. Ditunno, J W Little, A Tessler, A S Burns
    Abstract:

    Spinal Shock has been of interest to clinicians for over two centuries. Advances in our understanding of both the neurophysiology of the Spinal cord and neuroplasticity following Spinal cord injury have provided us with additional insight into the phenomena of Spinal Shock. In this review, we provide a historical background followed by a description of a novel four-phase model for understanding and describing Spinal Shock. Clinical implications of the model are discussed as well.

  • the pattern of reflex recovery during Spinal Shock
    Spinal Cord, 1999
    Co-Authors: John F. Ditunno, V Graziani, James W Little
    Abstract:

    Study Design: A prospective descriptive study of the course of recovery of reflexes following acute Spinal cord injury (SCI). Objectives: The purpose of the study was to observe the pattern of reflex recovery following acute SCI in order to determine the prognostic significance of reflexes for ambulation and their relationship to Spinal Shock. Setting: A regional Spinal cord injury center in Philadelphia, Pennsylvania, USA. Methods: Fifty subjects admitted consecutively over a 9 month period and on the day of injury were observed for the following reflexes; bulbo-cavernosis (BC), delayed plantar response (DPR), cremasteric (CRM), ankle jerk (AJ), knee jerk (KJ), and normal plantar response for 5–7 days a week and 6–8 weeks duration. The 50 subjects were assessed for ambulation of 200 feet at time of discharge. MRI studies were reviewed on 13/28 complete (ASIA A) injuries. Results: Thirty-five subjects (28 ASIA A, 4 ASIA B, 3 ASIA C) had a DPR of 2 days or longer duration and these subjects were not ambulatory. The fourteen subjects (12 ASIA D and 2 ASIA C), who were ambulatory, either had no DPR (11/14) or had a DPR of only 1 days duration (3/14). One subject (ASIA B) was not ambulatory and had a DRP of 1 days duration. The DPR was the first reflex to recover most often, followed by the BC, CRM in the first few days and later followed by the deep tendon reflexes (AJ & KJ) by 1–2 weeks respectively. Less than 8% of subjects had no reflexes on the day of injury and the reflexes did not follow a caudal-rostral pattern of recovery. Conclusions: Prognosis for ambulation based on reflexes early after SCI should not be linked to current descriptions of Spinal Shock. In fact, the view of Spinal Shock, based on the absence of reflexes and the recovery of reflexes in a caudal to rostral sequence, is of limited clinical utility and should be discarded. The evolution of reflexes over several days following injury may be more relevant to prognosis than the use of the term Spinal Shock and the presence or absence of reflexes on the day of injury.

  • incomplete Spinal cord injury neuronal mechanisms of motor recovery and hyperreflexia
    Archives of Physical Medicine and Rehabilitation, 1999
    Co-Authors: James W Little, John F. Ditunno, Steven A. Stiens, Roge M Harris
    Abstract:

    Abstract Objective: To understand neuronal mechanisms of motor recovery and hyperreflexia after incomplete Spinal cord injury (SCI), and their role in rehabilitation. Design: Reviewed and compared clinical, neurophysiologic, and neuropathologic data from human SCI patients with behavioral, neurophysiologic, and neuroanatomic data from animals to postulate underlying neuronal mechanisms. Outcome: A postulation that two neuronal mechanisms—receptor up-regulation and synapse growth—act sequentially, to explain the gradual appearance of motor recovery after incomplete SCI. These same mechanisms may also act in Spinal reflex pathways to mediate hyperreflexia caudal to SCI. Results: After incomplete SCI, walking ability and hyperreflexia often develop. Initially, cord neurons are hyperpolarized and less excitable because of loss of normal descending facilitation; this is Spinal Shock. Then, gradually, voluntary movement recovers and hyperreflexia develops. Early (hours to days), these changes develop simultaneously, suggesting a common postsynaptic mechanism—likely, an increase in postsynaptic receptor excitability, possibly receptor up-regulation. Late (weeks to months), recovery and reflex changes occur at a slow rate, are no longer simultaneous, and are long-lasting, which suggests a presynaptic mechanism, such as local synapse growth in spared descending pathways and in reflex pathways. This presumed synapse growth is seemingly enhanced by active use of the growing pathway. Also, developing hyperreflexia appears to limit motor recovery. Conclusions: These observations suggest that rehabilitation for incomplete SCI should (1) increase activity in spared descending motor pathways, (2) initially use reflex facilitation or central nervous system stimulants to assist spared descending inputs in depolarizing cord neurons, and (3) later minimize reflex input, when spared descending inputs can depolarize cord neurons without reflex facilitation. Better understanding of neuronal mechanisms that underlie motor recovery after incomplete SCI promises better outcomes from rehabilitation.

James W Little - One of the best experts on this subject based on the ideXlab platform.

  • the pattern of reflex recovery during Spinal Shock
    Spinal Cord, 1999
    Co-Authors: John F. Ditunno, V Graziani, James W Little
    Abstract:

    Study Design: A prospective descriptive study of the course of recovery of reflexes following acute Spinal cord injury (SCI). Objectives: The purpose of the study was to observe the pattern of reflex recovery following acute SCI in order to determine the prognostic significance of reflexes for ambulation and their relationship to Spinal Shock. Setting: A regional Spinal cord injury center in Philadelphia, Pennsylvania, USA. Methods: Fifty subjects admitted consecutively over a 9 month period and on the day of injury were observed for the following reflexes; bulbo-cavernosis (BC), delayed plantar response (DPR), cremasteric (CRM), ankle jerk (AJ), knee jerk (KJ), and normal plantar response for 5–7 days a week and 6–8 weeks duration. The 50 subjects were assessed for ambulation of 200 feet at time of discharge. MRI studies were reviewed on 13/28 complete (ASIA A) injuries. Results: Thirty-five subjects (28 ASIA A, 4 ASIA B, 3 ASIA C) had a DPR of 2 days or longer duration and these subjects were not ambulatory. The fourteen subjects (12 ASIA D and 2 ASIA C), who were ambulatory, either had no DPR (11/14) or had a DPR of only 1 days duration (3/14). One subject (ASIA B) was not ambulatory and had a DRP of 1 days duration. The DPR was the first reflex to recover most often, followed by the BC, CRM in the first few days and later followed by the deep tendon reflexes (AJ & KJ) by 1–2 weeks respectively. Less than 8% of subjects had no reflexes on the day of injury and the reflexes did not follow a caudal-rostral pattern of recovery. Conclusions: Prognosis for ambulation based on reflexes early after SCI should not be linked to current descriptions of Spinal Shock. In fact, the view of Spinal Shock, based on the absence of reflexes and the recovery of reflexes in a caudal to rostral sequence, is of limited clinical utility and should be discarded. The evolution of reflexes over several days following injury may be more relevant to prognosis than the use of the term Spinal Shock and the presence or absence of reflexes on the day of injury.

  • incomplete Spinal cord injury neuronal mechanisms of motor recovery and hyperreflexia
    Archives of Physical Medicine and Rehabilitation, 1999
    Co-Authors: James W Little, John F. Ditunno, Steven A. Stiens, Roge M Harris
    Abstract:

    Abstract Objective: To understand neuronal mechanisms of motor recovery and hyperreflexia after incomplete Spinal cord injury (SCI), and their role in rehabilitation. Design: Reviewed and compared clinical, neurophysiologic, and neuropathologic data from human SCI patients with behavioral, neurophysiologic, and neuroanatomic data from animals to postulate underlying neuronal mechanisms. Outcome: A postulation that two neuronal mechanisms—receptor up-regulation and synapse growth—act sequentially, to explain the gradual appearance of motor recovery after incomplete SCI. These same mechanisms may also act in Spinal reflex pathways to mediate hyperreflexia caudal to SCI. Results: After incomplete SCI, walking ability and hyperreflexia often develop. Initially, cord neurons are hyperpolarized and less excitable because of loss of normal descending facilitation; this is Spinal Shock. Then, gradually, voluntary movement recovers and hyperreflexia develops. Early (hours to days), these changes develop simultaneously, suggesting a common postsynaptic mechanism—likely, an increase in postsynaptic receptor excitability, possibly receptor up-regulation. Late (weeks to months), recovery and reflex changes occur at a slow rate, are no longer simultaneous, and are long-lasting, which suggests a presynaptic mechanism, such as local synapse growth in spared descending pathways and in reflex pathways. This presumed synapse growth is seemingly enhanced by active use of the growing pathway. Also, developing hyperreflexia appears to limit motor recovery. Conclusions: These observations suggest that rehabilitation for incomplete SCI should (1) increase activity in spared descending motor pathways, (2) initially use reflex facilitation or central nervous system stimulants to assist spared descending inputs in depolarizing cord neurons, and (3) later minimize reflex input, when spared descending inputs can depolarize cord neurons without reflex facilitation. Better understanding of neuronal mechanisms that underlie motor recovery after incomplete SCI promises better outcomes from rehabilitation.

Roge M Harris - One of the best experts on this subject based on the ideXlab platform.

  • incomplete Spinal cord injury neuronal mechanisms of motor recovery and hyperreflexia
    Archives of Physical Medicine and Rehabilitation, 1999
    Co-Authors: James W Little, John F. Ditunno, Steven A. Stiens, Roge M Harris
    Abstract:

    Abstract Objective: To understand neuronal mechanisms of motor recovery and hyperreflexia after incomplete Spinal cord injury (SCI), and their role in rehabilitation. Design: Reviewed and compared clinical, neurophysiologic, and neuropathologic data from human SCI patients with behavioral, neurophysiologic, and neuroanatomic data from animals to postulate underlying neuronal mechanisms. Outcome: A postulation that two neuronal mechanisms—receptor up-regulation and synapse growth—act sequentially, to explain the gradual appearance of motor recovery after incomplete SCI. These same mechanisms may also act in Spinal reflex pathways to mediate hyperreflexia caudal to SCI. Results: After incomplete SCI, walking ability and hyperreflexia often develop. Initially, cord neurons are hyperpolarized and less excitable because of loss of normal descending facilitation; this is Spinal Shock. Then, gradually, voluntary movement recovers and hyperreflexia develops. Early (hours to days), these changes develop simultaneously, suggesting a common postsynaptic mechanism—likely, an increase in postsynaptic receptor excitability, possibly receptor up-regulation. Late (weeks to months), recovery and reflex changes occur at a slow rate, are no longer simultaneous, and are long-lasting, which suggests a presynaptic mechanism, such as local synapse growth in spared descending pathways and in reflex pathways. This presumed synapse growth is seemingly enhanced by active use of the growing pathway. Also, developing hyperreflexia appears to limit motor recovery. Conclusions: These observations suggest that rehabilitation for incomplete SCI should (1) increase activity in spared descending motor pathways, (2) initially use reflex facilitation or central nervous system stimulants to assist spared descending inputs in depolarizing cord neurons, and (3) later minimize reflex input, when spared descending inputs can depolarize cord neurons without reflex facilitation. Better understanding of neuronal mechanisms that underlie motor recovery after incomplete SCI promises better outcomes from rehabilitation.

Johannes Noth - One of the best experts on this subject based on the ideXlab platform.

  • what if anything is Spinal Shock
    JAMA Neurology, 1999
    Co-Authors: W Nacimiento, Johannes Noth
    Abstract:

    The term Spinal Shock describes the sudden and transient suppression of neural functions below the level of acute Spinal cord lesions, usually in the setting of trauma, ischemia, hemorrhage, or inflammatory diseases. The syndrome of Spinal Shock primarily refers to motor and autonomic disorders (see Young and Woolsey 1 and Guttmann 2 for reviews) mediated by the reduced excitability of Spinal neurons following disconnection from descending input. 3 During this state, a flaccid paralysis of skeletal muscles occurs, and all tendon, cutaneous, and autonomic reflexes integrated in the Spinal cord below the lesion are abolished or greatly reduced. Following variable periods of time, from several days up to 4 to 6 weeks, Spinal reflexes return and eventually become exaggerated as the syndrome of spasticity develops (see Noth 4 for review).