Stroke is a leading cause of disability in the United States.1 The Veterans Health Administration (VHA) of the Department of Veterans Affairs (VA) estimates that 15 000 veterans are hospitalized for stroke each year (VA HSR&D, 1997).

Forty percent of stroke patients are left with moderate functional impairments and 15% to 30% with severe disability.2 Effective rehabilitation interventions initiated early after stroke can enhance the recovery process and minimize functional disability. Improved functional outcomes for patients also contribute to patient satisfaction and reduce potential costly long-term care expenditures.

There are only 45 rehabilitation bed units (RBUs) in the VA today. Many veterans who have a stroke and are admitted to a VA Medical Center will find themselves in a facility that does not offer comprehensive, integrated, multidisciplinary care. In a VA rehabilitation field survey published in December 2000, more than half of the respondents reported that the “rehabilitative care of stroke patients was incomplete, fragmented, and not well coordinated” at sites lacking a RBU (VA Stroke Medical Rehabilitation Questionnaire Results, 2000).

In Department of Defense (DoD) medical treatment facilities, approximately 20 000 active-duty personnel and dependents were seen in 2002 for stroke and stroke-related diagnoses according to ICD-9 coding.3 Comprehensive treatment for stroke patients in DoD medical facilities is given primarily at medical centers. Smaller DoD community hospitals may have limited resources to see both inpatients and outpatients, relying more on the TRICARE network for ongoing stroke rehabilitation services.

A growing body of evidence indicates that patients do better with a well-organized, multidisciplinary approach to post-acute rehabilitation after a stroke.4–6 The VA/DoD Stroke Rehabilitation Working Group only focused on the post–acute stroke rehabilitation care.

Duncan and colleagues7 found that greater adherence to post-acute stroke rehabilitation guidelines was associated with improved patient outcomes and concluded “compliance …

/pdf/management-of-adult-stroke-rehabilitation-care-a-clinical-55zu3naq5e.pdf

Management of Adult Stroke Rehabilitation Care: a clinical practice guideline.

Vesicourethral dysfunction is very frequent in multiple sclerosis (MS) and has functional consequences for patients' quality of life and also an organic impact following complications of the neurogenic bladder on the upper urinary tract. While the functional impact and its management are well documented in the literature, the organic impact remains underestimated and there are no consensual practical guidelines for the screening and prevention of MS neurogenic bladder complications. The aim of this review of the literature, focused on identifying the risk factors of urinary tract complications in MS, is to put forward well informed considerations to help in the definition of practical guidelines for the follow-up of the neurogenic bladder in MS in order to improve its prevention and patient management. Four main risk factors have been identified for upper urinary tract damage: the duration of MS, the presence of an indwelling catheter, high-amplitude neurogenic detrusor contractions and permanent high detrusor pressure. Detrusor-sphincter dyssynergia, age over 50 and male sex may form three additional risk factors. Recommendations for long-term urological follow-up, taking into account these specific risks are constructed according to the procedures recommended by the French Health Authorities.

The neurogenic bladder in multiple sclerosis: review of the literature and proposal of management guidelines:

https://www.europeanurology.com/article/S0302-2838(07)01264-X/pdf

Botulinum Toxin A (Botox®) Intradetrusor Injections in Adults with Neurogenic Detrusor Overactivity/Neurogenic Overactive Bladder: A Systematic Literature Review

Several different drugs are now used, or are potentially useful, to treat patients with spasticity. Although these compounds vary in their actions on spinal neurons and reflex arcs, it is possible to formulate reasonable hypotheses regarding their modes of action. The benzodiazepines bind to specific benzodiazepine receptors linked to classic gamma-aminobutyric acid (GABA) receptors located on the terminals of primary afferent fibers. This binding results in an increased affinity of the GABA receptor for the amino acid, an augmented flux of chloride ions across the terminal membrane, and an increase in the amount of presynaptic inhibition. Baclofen activates GABAB receptors putatively located on the same terminals. Activation of these receptors retards the influx of calcium ions into the terminals, thereby reducing the evoked release of excitatory amino acids and possibly other transmitters. Progabide and its metabolites act on both classic and GABAB receptors. Glycine works on specific inhibitory receptors located on spinal interneurons and motoneurons. The phenothiazines act on the brainstem to alter the function of fusimotor fibers. Phenytoin and carbamazepine reduce the afferent output of muscle spindles. Dantrolene diminishes the activation of the contractile process in muscle fibers by reducing the release of calcium ions from the sarcoplasmic reticulum. This review summarizes the data supporting these concepts.

Antispasticity drugs: mechanisms of action.

One hundred and seventy patients with multiple sclerosis and bladder dysfunction were evaluated. Emphasis was placed on the relationship between their neurological features and urinary symptoms. The severity of the urinary symptoms was related to the degree of pyramidal impairment in the lower limbs so that both problems are thought to reflect the extent of spinal involvement. No other neurological features correlated with bladder dysfunction. Detrusor hyperreflexia was the commonest finding on cystometry and no patient had areflexia. More than half of the patients had a significantly raised post-micturition residual volume but symptoms were largely unreliable in predicting poor bladder emptying. In this series only two patients had evidence of upper tract disease: both men with severe, longstanding neurological disease who had indwelling catheters. Detrusor hyperreflexia can be anticipated in patients with MS who have irritative urinary symptoms and pyramidal signs in their lower limbs. After measurement of the residual volume appropriate treatment can be instituted.

https://jnnp.bmj.com/content/jnnp/56/3/245.full.pdf

Urinary symptoms and the neurological features of bladder dysfunction in multiple sclerosis.

In 27 patients with multiple sclerosis (MS), and in 10 control subjects of comparable age, percent ideal body weight and sex ratio, the cerebrospinal fluid (CSF) content of somatostatin was measured by radioimmunoassay. The results showed that the group of patients in relapse (n = 16) had significantly lower somatostatin content in CSF (95 +/- 4.1 (SEM) pg/ml) than both the control group (142 +/- 8.4 pg/ml) and the group of MS patients (n = 11), who had been in a clinical stable phase for more than 6 months (131 +/- 3.2 pg/ml). Duration of the disease and degree of neurological impairment were apparently without relation to the reduction of somatostatin content in the CSF. There was no relationship between CSF content of somatostatin and the content of total protein or IgG, neither of which showed any relationship to the activity of the disease.

Low somatostatin content in cerebrospinal fluid in multiple sclerosis. An indicator of disease activity

There is every reason to continue the search for compounds which exert a beneficial effect on spasticity, both because improved possibilities of treatment are desirable and because such compounds may be conducive to elucidating the pathophysiological mechanisms of spasticity. In the course of time, a great variety of agents have been given a trial; and since 1954 when Florey reported that extract from mammalian brain contained a neuro-inhibitory substance, such agents have attracted great attention. This applies, in particular, to gamma-aminobutyric acid (GABA) , which has been shown to be the active principle in Florey's extract (Bazemore et al. 1956, 1957). GABA has been assumed to be the transmitter substance at the inhibitory synapses ; but this problem has not yet been clarified. It would be reasonable to study the effect of GABA on spasticity; but as the blood-brain barrier is relatively impermeable to GABA, it is difficult to administer to human beings. The search has therefore been continued for GABA-like substances which more easily cross the blood-brain barrier, preferably agents which can be administered orally. The GABA derivative p(4-chloropheny1)-y-aminobutyric acid is such a substance, and studies of it are reported below.

Gaba derivative in spasticity. (Beta-(4-chlorophenyl)-gamma-aminobutyric acid, Ciba 34.647-Ba).

Baclofen is chemically related to GABA and has proved to have a clinical effect on spasticity and on flexor spasms. The mode of action of baclofen was studied by quantitative measurements of some reflexes and of voluntary power in relation to intravenous injections of the drug (average dose 0.38 mg per kg body weight) in 44 patients with spasticity due to spinal or cerebral lesion or multiple sclerosis; a total of 53 injections were given. In most of the patients studied, depression occurred in the phasic stretch reflex (Achilles tendon), tonic stretch reflex, flexor reflex, reflexes from the pelvic floor and in the tonic vibration reflex; whereas the fl reflex changed in only a few cases, and voluntary power did not change at all. In some patients a pronounced increase was observed in the vibration-induced depression of the H reflex, which after baclofen approached normal. Baclofen can reduce the fusimotor drive, whereas a general primary effect on the α motoneurones is unlikely. It acts on the interneurones and can increase ‘presynaptic’ inhibition of the la nerve fibres. It is capable of exerting its action exclusively at the spinal level and can depress hyperactive stretch reflexes, whether they are caused by a spinal or cerebral lesion.

The mode of action of the gaba derivative baclofen in human spasticy

— During a period of 2 1/2 years, 198 patients with definite MS were admitted to our neurological department. 88 were investigated neurourodynamically because of distinct voiding dysfunction. 73 patients showed detrusor hyperreflexia, 14 detrusor hyporeflexia or areflexia and one had normal findings. There was no obvious correlation between the occurrence of the symptoms, irritative and obstructive, and the allocation of the patients into different cystometric groups. The predominant symptom was urge incontinence. More men had been treated or were permanently treated with intravesical catheter, but mean residual urine did not show any sex difference. In 36 patients with detrusor hyperreflexia, dyssynergia was observed and was classified into 3 groups. In the group with clonic sphincter EMG activity during voiding, 5 of the patients had dyssynergia because of flexor spasms transmitted to the sphincter. In patients with dyssynergia characterized by increased sphincter activity throughout detrusor contraction, a large mean residual urine was noted, but dyssynergia did not always prevent acceptable emptying. A low rate of complication in the upper urinary tract was observed. Treatment is discussed.

Neurourodynamic evaluation of voiding dysfunction in multiple sclerosis.

In a double-blind cross-over trial of two 2-week periods, the clinical effect of progabide was compared to placebo. 16 patients with spasticity in a stationary phase completed the trial. 14 had multiple sclerosis, 2 hereditary spastic paraplegia. 5 were female and 11 male. The median age was 45.5 years (range 30-62 years). The median daily dosage of progabide was 24.3 mg/kg (range 14.3-32.7 mg/kg). During progabide treatment, there was a reduction in spastic hypertonia (P less than 0.01), a suppression of tendon reflexes (patellar) (P less than 0.01), and a reduction in the frequency of flexor spasms (P less than 0.05). No significant changes in voluntary power were registered. The global clinical impression revealed a therapeutic effect in 87% of the patients (95% confidence limits 61-98%). The improvement was judged as medium or important in 50% of the patients (95% confidence limits 23-77%). No side-effects or laboratory abnormalities were seen.

The clinical effect of the GABA-agonist, progabide, on spasticity.

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