Extensor truncal dystonia: successful treatment with botulinum toxin injections

An alternative method of determining the integrated input function, necessary in the quantitative [18F]fluorodeoxyglucose (FDG) autoradiographic model, has been developed. Using erythrocytes as reference tissue, researchers require only one blood sample after injection of FDG to obtain the integrated input function. METHODS: The amount of FDG-6-PO4 in the erythrocytes is proportional to their exposure to FDG, that is, the integrated input function. Free FDG is removed by washing the erythrocytes twice. Inter- and intraindividual differences of the metabolic rate of erythrocytes are corrected for by an in vitro incubation with a known amount of FDG. RESULTS: Validation of the proposed method was done by correlating the integrated input function, based on the glucose metabolism of the erythrocytes, to the integrated input function obtained by multiple venous blood samples. The new method provides the integrated input function with an accuracy better than +/-8%. CONCLUSION: By using erythrocytes as a reference tissue, researchers can determine the integrated input function in the quantitative FDG autoradiographic model with an accuracy sufficient for clinical PET studies. The simplicity of the method also makes it suitable for FDG studies on small children. With two samples, the method can also be used for a simplified graphical Patlak analysis.     

Nerve injection injury with botulinum toxin

The therapeutic use of botulinum toxin (Botox) is increasing in popularity. Previous studies have shown that various drugs, especially when injected intrafascicularly, can cause major nerve damage. This study evaluates the potential for neurotoxicity of botulinum toxin in a rat sciatic nerve model. Lewis rats were randomly assigned to one of six groups (n = 10/group). Group 1, 2, and 3 rats received, respectively, an intrafascicular, extrafascicular, and extraneural injection of 50 microl of botulinum toxin (50 UI/ml). Group 4, 5, and 6 rats received 50 microl of 10% phenol as a positive control. Five animals received saline as a negative control. Animals were sacrificed at 2 and 7 weeks. Nerves were harvested and processed for histology and morphometry. Nerves in all botulinum toxin groups retained a normal architecture without cellular infiltration or demyelination. The number and diameter of fibers, the thickness of myelin, and the percentage of neural tissue were comparable with normal controls. Nerves injected intraneurally with phenol presented with severe damage, demyelination, and inflammation at 2 weeks and showed signs of early regeneration at 7 weeks. This study demonstrates that in a rat model, even direct intraneural injection of botulinum toxin caused no damage. This information should encourage the reconstructive surgeon to consider broader applications of this drug.     

Chlorpropamide-induced hypoglycemia: successful treatment with diazoxide

A healthy adolescent boy was treated on two occasions for an overdose of chlorpropamide (Diabinese). Glucose therapy alone was not sufficient to control the hypoglycemia, but the administration of glucose plus diazoxide raised the blood sugar to supranormal levels. A bolus of intravenous glucagon briefly raised the blood sugar level to within normal limits, increased the blood ketones but also augmented insulin secretion. An overdose of sulfonylurea may cause prolonged and fatal hypoglycemia. Rational therapy, both in diabetic and normal persons, is glucose plus an "insulin antagonist." The administration of diazoxide was effective in our patient, substantially reducing the plasma insulin level; this agent may be the "insulin-antagonist" of choice for use in sulfonylurea-induced hypoglycemia.     

Neuropsychological impairments after spinal cord injury: A comparative study with mild traumatic brain injury.

Objective: To determine if individuals with mild traumatic brain injury (MTBI) perform differently on neuropsychological measures than individuals with spinal cord injury (SCI) having no loss of consciousness. Design and Participants: Data were collected prospectively on 33 matched pairs of individuals with SCI or MTBI. Independent t tests were performed to identify differences between the SCI and MTBI groups. Results: Although those with SCI generally outperformed individuals with MTBI, no meaningful between-groups differences were noted on 5 of the 10 neuropsychological tests administered. Greater than 40% of the SCI patients were identified as having impairments in processing speed, motor speed, and verbal learning. Conclusions: Treatment planning after SCI should include procedures to identify cognitive deficits that may complicate adjustment to disability and delay acquisition of new skills. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Increased mortality after successful treatment for Hodgkin's disease

PURPOSE: To determine the impact of treatment toxicity on long-term survival in pediatric Hodgkin's disease. PATIENTS AND METHODS: We studied late events in 387 patients treated for pediatric Hodgkin's disease on four consecutive clinical trials at St Jude Children's Research Hospital from 1968 to 1990. Relative risks, actuarial risks, and absolute excess risks for cause-specific deaths were calculated. RESULTS: As of April 1997, 316 (82%) of patients were alive, with a median follow-up of 15.1 (range, 2.9 to 28.6) years. In this cohort, which represented 5,623 person-years of follow-up, 71 fatal events resulted from Hodgkin's disease (n=36), second malignancies (n=14), infections (n=7), accidents (n=7), cardiac disease (n=6), and asphyxiation (n=1). The 5-year estimated event-free survival (EFS) for the entire cohort was 79.6%+/-2.1 %, which declined to 63.1%+/-4.4% by 20 years. Cumulative incidences of cause-specific deaths at 25 years were 9.8%+/-1.6% for Hodgkin's disease, 8.1%+/-2.6% for second malignancy, 4.0%+/-1.8% for cardiac disease, 3.9%+/-1.5% for infection, and 2.1%+/-0.8% for accidents. Standardized incidence ratios showed excess risk for all second malignancies (12; 95% confidence interval [CI], 8 to 17), acute myeloid leukemia (81; 95% CI, 16 to 237), solid tumors (11; 95% CI, 7 to 16), and breast cancer (33; 95% CI, 12 to 72). Standardized mortality ratios also showed excess mortality from cardiac disease (22; 95% CI, 8 to 48) and infection (18; 95% CI, 7 to 38). CONCLUSION: Compared with age- and sex-matched control populations, survivors of pediatric Hodgkin's disease who were treated before 1990 face an increased risk of early mortality related to second cancers, cardiac disease, and infection.     

Multifamily group treatment for veterans with traumatic brain injury.

A common clinical problem encountered by clinicians treating veterans who incurred traumatic brain injury (TBI) while serving in Afghanistan in support of Operation Enduring Freedom (OEF) or in Iraq in support of Operation Iraqi Freedom (OIF) is lack of knowledge about TBI on the part of the veterans' family members. Insufficient information can exacerbate marital or family conflict and lead to psychological distress and social isolation for the veteran and family, and suboptimal illness management for the veteran. To address this problem, we adapted Multifamily Group Treatment (MFGT), an evidence-based practice for treatment of serious mental illness (SMI), for treatment of OEF/OIF veterans with TBI and their families. We have implemented the adapted treatment (MFG-TBI) in four groups of veterans and families (N = 20 veterans and 20 family members) across two sites: the Durham VA Medical Center (VAMC) in North Carolina and the JJ Peters VAMC in the Bronx, New York. Adaptations focused on contents and format of the educational components, specification of a protocol for conjugal couples, and the addition of an ecomap to identify support systems during the joining (i.e. assessment) phase, a shorter (9 months) intervention duration, and a more active clinician role including use of motivational enhancement, intersession support, and coordination with other service providers. Biweekly group sessions were supervised and rated for adherence. We illustrate how MFG-TBI both educates and builds problem-solving skills with clinical examples. Suggestions for effective use of problem-solving skills with this population are offered. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Repeatedly successful closure of the larynx for the treatment of chronic aspiration with the use of botulinum toxin A

Botulinum toxin A was used preoperatively to temporarily paralyze the intrinsic laryngeal muscles to hinder movements during the healing period after operation. In addition, toxin was injected into the cricopharyngeal muscle to allow a better passive drainage of the saliva into the esophagus. We treated six patients. Three suffered from chronic aspiration problems after multiple lower cranial nerve lesions, and three patients were apallic (after stroke and major brain injury). Two weeks before scheduled operation, we injected the toxin into the posterior cricoarytenoid muscles, the aryepiglottic muscles, and the vocalis muscle on both sides, as well as the cricopharyngeal muscle. The amount of injected toxin varied between 1.0 and 1.4 mL, equal to 200 to 280 units of botulinum toxin A (Dysport). After a complete palsy of these muscles (controlled by direct electromyography), a closure of the larynx was performed. After laminotomy and exposure of the intralaryngeal structures, the false vocal cords were mobilized and adapted with sutures. Because involuntary movements of the intralaryngeal musculature were absent, primary healing without complications occurred in all cases. Aspiration and related complications disappeared in all patients. In addition, the intensity of patient care could be considerably reduced. Preoperative use of botulinum toxin A allows sufficient laryngeal closure. This procedure is especially useful in the treatment of children and young adults, preserving the ability of later speech rehabilitation because of the return of voluntary movements of the intrinsic laryngeal muscles 6 months after the injection. Furthermore, this technique, as minimal surgical intervention, can be performed in high-risk patients.     

Rehabilitation after traumatic brain injury in adults

PURPOSE: Traumatic brain injury (TBI) stands as a major public health problem and one of the most important challenges for neurological rehabilitation. This review discusses advances that have occurred in the past 10 years in rehabilitation after severe TBI in adults. METHOD: First, theoretical concepts, goals of rehabilitation and organization of resources are reviewed. Then specific questions that arise in the rehabilitation of severe TBI patients are considered. RESULTS: Three phases are distinguished in post-traumatic evolution. Acute rehabilitation takes place during coma and arousal states. Specific aims are to prevent orthopaedic and visceral complications, and to provide sensory stimulations with the hope of accelerating arousal. Secondly subacute (generally inpatient) rehabilitation is designed to facilitate and accelerate recovery of impairments, and to compensate for disabilities. Motility, cognition, behaviour, personality and affect should be simultaneously addressed in an holistic approach. Physical as well as psychological independence and self-awareness are the major goals to emphasize. A third, post-acute rehabilitation phase includes outpatient therapy for achieving physical, domestic and social independence, reduction of handicaps and re-entry into the community. CONCLUSIONS: Problems with returning home, obtaining financial independence, driving, returning to work, participating in social relationships and leisure activities, and the importance of psychosocial adjustment and self-acceptance, are outlined. Questions about economic aspects and rehabilitation in the future are addressed.     

Neurochemical mechanisms in brain injury and treatment: a review

This article reviews cellular energy transformation processes and neurochemical events that take place at the time of brain injury and shortly thereafter emphasizing hypoxia-ischemia, cerebrovascular accident, and traumatic brain injury. New interpretations of established concepts, such as diffuse axonal injury, are discussed; specific events, such as free radical production, excess production of excitatory amino acids, and disruption of calcium homeostasis, are reviewed. Neurochemically-based interventions are also presented: calcium channel blockers, excitatory amino acid antagonists, free radical scavengers, and hypothermia treatment. Concluding remarks focus on the role of clinical neuropsychologists in validation of treatment interventions.     

Delayed traumatic cerebral aneurysm after brain injury

Traumatic aneurysms (TAs) are an unusual etiology for late neurological deterioration after traumatic brain injury (TBI) and represent less than 1% of all cerebral aneurysms. TAs most often are diagnosed acutely but may be delayed in presentation. To increase awareness of this serious but treatable condition when diagnosed early, we report a delayed TA after a motor vehicle accident. The patient experienced a seizure on day 46 postinjury while in rehabilitation and demonstrated persistent lethargy and hemiparesis. Neuroimaging revealed a large, ruptured left pericallosal artery TA, which was surgically clipped. The patient completed his rehabilitation course and was eventually discharged home with family. Among TBIs, TAs are associated with penetrating injuries and skull base or anterior cranial fossa fractures. Associated mortality is high, especially if rupture has occurred. Although TAs are rare, the clinician should be vigilant in the at-risk patient.     

Varieties of deficit unawareness after brain injury

The failure to recognize the existence of disease is known as anosognosia. This article provides a brief discussion of the evolution of this concept and reviews some qualitative differences in the manner in which the disavowal of neurogenic impairment is expressed. Theoretical explanations for the unawareness of deficit after neurologic illness include motivational-symbolic, cognitive subsystem, and supraordinate system theories. Observations from a clinically derived, structured awareness interview are presented, suggesting three factors that may underlie patients' apparent lack of awareness of deficits after traumatic brain injury. These include diminished awareness of deficits secondary to impaired cognition, especially memory and reasoning deficits; psychological reactance and denial of deficits; and a relatively "pure" inability to recognize areas of impaired functioning as a direct consequence of brain injury. The causes of unawareness are likely to be complex and multiply determined in any given patient, although it may be possible to identify primary, secondary, and even tertiary contributions according to specific behavioral and phenomenological characteristics. The ability of patients to modify their perceptions and acknowledgment of deficits after objective feedback may have particular diagnostic value and clinical utility in this regard.     

Association of adhesive macromolecules with terminal sprouts at the neuromuscular junction after botulinum treatment

Small quantities of botulinum toxin (BTX) are useful in the treatment of certain movement disorders, such as laryngeal spasmodic dysphonia, blepharospasm, and cervical dystonia. However, the corrective paralytic effects of BTX are only temporary, in part because of the formation of remodeled neuromuscular junctions. Here, we questioned whether various factors within and near the neuromuscular junction could contribute to the remodeling seen after BTX treatment. BTX was injected subcutaneously in the region of the levator auris longus muscle. At 1-week intervals, levator auris longus muscles were removed and examined histochemically. As previously described, BTX treatment results in a progressive elongation of end plates. The neural cell adhesion molecule was not associated with the elongated end plates but was associated with the BTX-induced nerve sprouts after long intervals (3 to 4 weeks). Similarly, after BTX, laminin-1 (composed of alpha 1, beta 1, and gamma 1 chains) reactivity was associated with the nerve sprouts, but not with the end plates. Laminin beta 2 reactivity at the end plate dispersed somewhat within 1 week but remained diffusely associated with the elongating end plates for up to 5 weeks. Together these results suggest that neural cell adhesion molecule and laminins may participate in the sprouting observed after BTX treatment and that alterations in laminin beta 2 expression may participate in initial loss of contacts.     

Spontaneous output of acetylcholine from rat diaphragm preparations declines after treatment with botulinum toxin

A gas chromatographic spectrometric assay was used to measure tissue and released acetylcholine and choline in diaphragm preparations of rats previously injected with botulinum toxin type A. Botulinum intoxication was found not to alter the acetylcholine content of rat diaphragms in vivo or in fully paralyzed muscles in vitro. This result provides direct support for the hypothesis that botulinum toxin blocks transmitter release without affecting acetylcholine synthesis. However, in diaphragm preparations in vitro, this toxin was found to inhibit not only the evoked release of acetylcholine but also the spontaneous "leakage" of acetylcholine that is measured at rest. Additional experiments were performed to characterize this action of the toxin. The magnitude of the decline in resting acetylcholine output appears to be too large to be accounted for solely by the known effect of botulinum toxin to reduce the frequency of miniature endplate potentials. The mechanism of this action of botulinum toxin remains an enigma.     

Vesiculobullous Hailey-Hailey disease: successful treatment with oral retinoids

A 56-year-old male presented with a pruritic, generalized vesiculobullous eruption. His past history revealed classical symptoms of limited Hailey-Hailey disease for 34 years. Clinically, vesicles, bullae and occasional pustules were present and multiple biopsies confirmed this to be an unusual presentation of Hailey-Hailey disease. Various therapeutic modalities including topical and oral antibiotics, oral prednisone and dapsone failed to achieve sustained remission. Treatment with low-dose oral etretinate (25 mg daily) produced marked clinical improvement with complete suppression of new vesicle formation after 6 weeks.     

Reduplicative paramnesia: Rehabilitation of content-specific delusion after brain injury.

ABSTRACT. Reduplicative paramnesia (RP) is one of several rare content-specific delusions that may be associated with specific central nervous system lesions and disease. RP involves the assertion that a geographic location exists simultaneously in more than one place. Correct identification of this syndrome and its neurological etiology is essential because misdiagnosing RP as a psychiatric disorder may lead to unnecessary use of neuroleptics and an increased risk of iatrogenic complications. The rehabilitation psychologist has an important role in treating the patient with RP, as well as educating family and other treating professionals regarding this syndrome. A case of RP arising from subarachnoid hemorrhage is presented with discussion of the rehabilitation course leading to the resolution of the RP. The neuropsychological and psychological underpinnings of RP are discussed, in addition to recommendations for rehabilitation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)