The Management and Rehabilitation of the Stroke Patient

1980 ◽  
Vol 25 (4) ◽  
pp. S41-S43
Author(s):  
J. Marshall
Keyword(s):  
Stroke Patient ◽  
Functional Disability ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Clinical Context ◽  
Neurological Defect

The residual neurological deficits after stroke are discussed in this article. The main problems are weakness, spasticity and rigidity. Weakness may be amenable to help with a variety of physical aids and mobility maintained with a wheelchair. Spasticity is defined in terms of the neurological defect and its consequences examined in the clinical context of the stroke patient. The place of antispastic drugs and their method of use is described. The importance of sensory loss in the production of functional disability is also discussed.

MRI Evaluation of Various Elbow, Forearm, and Wrist Neuropathies: A Pictorial Review

2021 ◽  
Vol 25 (04) ◽  
pp. 617-627
Author(s):  
Rola Husain ◽  
Arthi Reddy ◽  
Etan Dayan ◽  
Mingqian Huang ◽  
Idoia Corcuera-Solano
Keyword(s):  
Upper Extremity ◽  
Ulnar Nerve ◽  
Functional Disability ◽  
Carpal Tunnel Release ◽  
Calcium Pyrophosphate ◽  
Sensory Loss ◽  
Crystal Deposition ◽  
Entrapment Neuropathies ◽  
Pictorial Review ◽  
Mri Features

AbstractUpper extremity entrapment neuropathies are common and can cause pain, sensory loss, and muscle weakness leading to functional disability. We conducted a retrospective review from January 2007 until March 2020 of the magnetic resonance imaging (MRI) features of intrinsic and extrinsic causes of wrist, forearm, and elbow neuropathies of 637 patients who received a diagnosis of neuropathy by means of clinical and electrodiagnostic testing. We discuss cases with varying intrinsic and extrinsic nerve pathologies, including postoperative examples, affecting the median, radial, and ulnar nerve.Our collection of cases demonstrates a diversity of intrinsic and extrinsic causative factors. Intrinsic pathologies include neuritis as well as tumors arising from the nerve. Extrinsic causes resulting in nerve entrapment include masses, acute and chronic posttraumatic cases, anatomical variants, inflammatory and crystal deposition, calcium pyrophosphate deposition disease, and dialysis-related amyloidosis. Finally, we review postsurgical cases, such as carpal tunnel release and ulnar nerve transposition.Although upper extremity neuropathies tend to have a typical clinical presentation, imaging, particularly MRI, plays a vital role in evaluating the etiology and severity of each neuropathy and ultimately helps guide clinical management.

scholarly journals BMS-986020, a Specific LPA1 Antagonist, Provides Neuroprotection against Ischemic Stroke in Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1097
Author(s):  
Bhakta Prasad Gaire ◽  
Arjun Sapkota ◽  
Ji Woong Choi
Keyword(s):  
Ischemic Stroke ◽  
Survival Rate ◽  
Cell Apoptosis ◽  
Functional Disability ◽  
Brain Infarction ◽  
Tissue Loss ◽  
Neurological Deficits ◽  
Neuroprotective Effects ◽  
Acute Injuries

Stroke is a leading cause of death. Stroke survivors often suffer from long-term functional disability. This study demonstrated neuroprotective effects of BMS-986020 (BMS), a selective lysophosphatidic acid receptor 1 (LPA1) antagonist under clinical trials for lung fibrosis and psoriasis, against both acute and sub-acute injuries after ischemic stroke by employing a mouse model with transient middle cerebral artery occlusion (tMCAO). BMS administration immediately after reperfusion significantly attenuated acute brain injuries including brain infarction, neurological deficits, and cell apoptosis at day 1 after tMCAO. Neuroprotective effects of BMS were preserved even when administered at 3 h after reperfusion. Neuroprotection by BMS against acute injuries was associated with attenuation of microglial activation and lipid peroxidation in post-ischemic brains. Notably, repeated BMS administration daily for 14 days after tMCAO exerted long-term neuroprotection in tMCAO-challenged mice, as evidenced by significantly attenuated neurological deficits and improved survival rate. It also attenuated brain tissue loss and cell apoptosis in post-ischemic brains. Mechanistically, it significantly enhanced neurogenesis and angiogenesis in injured brains. A single administration of BMS provided similar long-term neuroprotection except survival rate. Collectively, BMS provided neuroprotection against both acute and sub-acute injuries of ischemic stroke, indicating that BMS might be an appealing therapeutic agent to treat ischemic stroke.

Surgical treatment of syringomyelia

1984 ◽  
Vol 61 (3) ◽  
pp. 531-538 ◽  
Author(s):  
Nicholas M. Barbaro ◽  
Charles B. Wilson ◽  
Philip H. Gutin ◽  
Michael S. B. Edwards
Keyword(s):  
Operative Therapy ◽  
Diagnostic Procedures ◽  
Clinical Findings ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Content Type ◽  
Neurological Improvement ◽  
Leg Stiffness ◽  
Fine Print

✓ The authors reviewed the clinical findings, radiological evaluation, and operative therapy of 39 patients with syringomyelia. Syringoperitoneal (SP) shunting was used in 15 patients and other procedures were used in 24 patients. Follow-up periods ranged from 1½ to 12 years. During the period of this study, metrizamide myelography in conjunction with early and delayed computerized tomography scanning replaced all other diagnostic procedures in patients with syringomyelia. Preoperative accuracy for the two procedures was 87%. The most common symptoms were weakness (79%), sensory loss (67%), pain (38%), and leg stiffness (28%). Surgery was most effective in stabilizing or alleviating pain (100%), sensory loss (81%), and weakness (74%); spasticity, headache, and bowel or bladder dysfunction were less likely to be reversed. Approximately 80% of patients with idiopathic and posttraumatic syringomyelia and 70% of those with arachnoiditis improved or stabilized. Better results were obtained in patients with less severe neurological deficits, suggesting the need for early operative intervention. A higher percentage of patients had neurological improvement with SP shunting than with any other procedure, especially when SP shunting was the first operation performed. Patients treated with SP shunts also had the highest complication rate, most often shunt malfunction. These results indicate that SP shunting is effective in reversing or arresting neurological deterioration in patients with syringomyelia.

scholarly journals Unique Surgical Issues in the Management of a Giant Retroperitoneal Schwannoma and Brief Review of Literature

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Santhosh Kuriakose ◽  
Syam Vikram ◽  
Surij Salih ◽  
Satheesan Balasubramanian ◽  
Nizamudeen Mangalasseri Pareekutty ◽  
...  
Keyword(s):  
Iliac Artery ◽  
Foot Drop ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Uneventful Recovery ◽  
Iliopsoas Muscle ◽  
Imaging Features ◽  
Diagnostic Dilemma ◽  
Internal Iliac ◽  
Retroperitoneal Schwannoma

Ancient Schwannoma, though benign, can cause diagnostic dilemma because of its clinical presentation and imaging features. We report the management of a giant retroperitoneal schwannoma in a 19-year-old young lady who presented with lower abdominal distension. CT scan reported a large heterogenous lesion in the abdominopelvic retroperitoneum (42 cm × 16 cm × 16 cm) as a malignant tumor. The unique problems we encountered were the enormous size, the location of major part of the tumor in the pelvis, the need for fertility preservation, the external iliac vessels stretching over the tumor making mobilization surgically demanding, and the prospects of neurological deficits. An en bloc resection of schwannoma with common iliac, external iliac and internal iliac veins, internal iliac artery, femoral and obturator nerves, and iliopsoas muscle was done maintaining oncological principles. External iliac artery that was cut to facilitate tumor mobilization was reanastomosed at the end of the procedure. Postoperatively patient had uneventful recovery with patchy sensory loss, foot drop, and quadriceps weakness which was rehabilitated with a foot drop splint and active physiotherapy.

Rehabilitation and management of apraxia after stroke

2001 ◽  
Vol 11 (2) ◽  
pp. 177-184 ◽  
Author(s):  
Caroline M van Heugten
Keyword(s):  
Stroke Patient ◽  
Neuropsychological Deficits ◽  
Sensory Loss

IntroductionA stroke patient puts on his shoes and then tries to put on his socks over his shoes. Entering the kitchen, this patient puts milk in the teapot, places the sugar bowl in the oven, and tries to drink from the milk jug. This patient is most probably apractic. Apraxia is one of the four classical neuropsychological deficits – such as agnosia, amnesia and aphasia – causing restrictions in the ability to carry out purposeful and learned activities. One of the first definitions of apraxia was given by Geschwind: ‘Disorders of the execution of learned movements which cannot be accounted for by either weakness, inco-ordination, or sensory loss, nor by incomprehension of, or inattention to commands.’

scholarly journals Management and outcome of spontaneous cervical epidural hematoma: Case report and review of the literature

2021 ◽  
Vol 12 (3) ◽  
pp. 094-097
Author(s):  
Yao Christian Hugues DOKPONOU ◽  
Adil BELHACHMI ◽  
Fernand Nathan IMOUMBY ◽  
Alngar DJIMRABEYE ◽  
Brahim El MOSTARCHID ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cervical Spinal Cord ◽  
Acute Attack ◽  
Cord Compression ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Neurologic Outcomes ◽  
Cord Injury ◽  
Spinal Cord Compression Syndrome

Spontaneous spinal epidural hematomas are rare and potentially disabling neurological emergencies. Its lead to devastating neurologic outcomes and most patient does not recover completely. The clinical presentation is diverse and includes a severe acute attack, radiating pain at the back, interscapular, or neurological deficits. We report a case of a young woman, 24-year-old, that was admitted to our department for sudden non-traumatic cervical spinal cord compression syndrome (Type A of the American Spinal Cord Injury Association “ASIA A”) including intense cervical back pain, sensory loss, and tetraplegia. Her past medical history was unremarkable. The MRI confirmed a cervical mass responsible for the spinal cord compression and the emergent surgical intervention allow us to evacuate acute C3-C7 hematoma. The patient never recovers from the neurologic deficit despite the emergent management of her case followed by functional musculoskeletal rehabilitation for two years.

scholarly journals Patterns of neurological deficits and recovery of postoperative C5 nerve palsy

2020 ◽  
Vol 33 (6) ◽  
pp. 742-750
Author(s):  
John K. Houten ◽  
Joshua R. Buksbaum ◽  
Michael J. Collins
Keyword(s):  
Japanese Orthopaedic Association ◽  
Decompressive Surgery ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Motor Deficit ◽  
C5 Palsy ◽  
Signal Change ◽  
The Mean ◽  
Signal Changes

OBJECTIVEParesis of the C5 nerve is a well-recognized complication of cervical spine surgery. Numerous studies have investigated its incidence and possible causes, but the specific pattern and character of neurological deficits, time course, and relationship to preoperative cord signal changes remain incompletely understood.METHODSRecords of patients undergoing cervical decompressive surgery for spondylosis, disc herniation, or ossification of the longitudinal ligament, including the C4–5 level, were reviewed from a 15-year period, identifying C5 palsy cases. Data collected included age, sex, diabetes and smoking statuses, body mass index, surgical levels, approach, presence of increased cord signal intensity, and modified Japanese Orthopaedic Association (mJOA) scores. Narrative descriptions of the patterns and findings on neurological examination were reviewed, and complications were noted. The minimum follow-up requirement for the study was 12 months.RESULTSOf 642 patients who underwent cervical decompressive surgery, 18 developed C5 palsy (2.8%). The incidence was significantly lower following anterior surgery (6 of 441 [1.4%]) compared with that following cervical laminectomy and fusion (12 of 201 [6.0%]) (p < 0.001). There were 10 men and 8 women whose mean age was 66.7 years (range 54–76 years). The mean preoperative mJOA score of 11.4 improved to 15.6 at the latest follow-up examination. There were no differences between those with and without C5 palsy with regard to sex, age, number of levels treated, or pre- or postoperative mJOA score. Fifteen patients with palsy (83%) had signal changes/myelomalacia on preoperative T2-weighted imaging, compared with 436 of 624 (70%) patients without palsy; however, looking specifically at the C4–5 level, signal change/myelomalacia was present in 12 of 18 (67%) patients with C5 palsy, significantly higher than in the 149 of 624 (24%) patients without palsy (p < 0.00003). Paresis was unilateral in 16 (89%) and bilateral in 2 (11%) patients. All had deltoid weakness, but 15 (83%) exhibited new biceps weakness, 8 (44%) had triceps weakness, and 2 (11%) had hand intrinsic muscle weakness. The mean time until onset of palsy was 4.6 days (range 2–14 days). Two patients (11%) complained of shoulder pain preceding weakness; 3 patients (17%) had sensory loss. Recovery to grade 4/5 deltoid strength occurred in 89% of the patients. No patient had intraoperative loss of somatosensory or motor evoked potentials or abnormal intraoperative C5 electromyography activity.CONCLUSIONSPostoperative C5 nerve root dysfunction appears in a delayed fashion, is predominantly a motor deficit, and weakness is frequently appreciated in the biceps and triceps muscles in addition to the deltoid muscle. Preoperative cord signal change/myelomalacia at C4–5 was a significant risk factor. No patient had a detectable deficit in the immediate postoperative period or changes in intraoperative neuromonitoring status. Neurological recovery to at least that of grade 4/5 occurred in nearly 90% of the patients.

scholarly journals Cauda equina schwannoma presenting with subarachnoid and subdural hemorrhage: Its underlying mechanism

2021 ◽  
Vol 12 ◽  
pp. 462
Author(s):  
Keitaro Shiraishi ◽  
Takahiro Tomita ◽  
Takuya Akai ◽  
Satoshi Kuroda
Keyword(s):  
Cauda Equina ◽  
Underlying Mechanism ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Subdural Hemorrhage ◽  
Intratumoral Hemorrhage ◽  
Acute Presentation ◽  
Spinal Subarachnoid Hemorrhage ◽  
Severe Back Pain ◽  
Spinal Schwannoma

Background: A patient presented with a spinal subarachnoid hemorrhage (SAH) and subdural hematoma (SDH) attributed to a spinal schwannoma at the T12-L1 level. Case Description: A 67-year-old male acutely presented with severe back pain and L1 paraparesis/sensory loss, with urinary incontinence. CT/MR studies showed a spinal SAH and SDH within a likely T12-L1 schwannoma. At surgery, the hemorrhage within the tumor was continuous through the lower pole of the tumor into the subarachnoid and subdural spaces; tumor was dissected away from the surrounding tissues and totally removed. The postoperative course was uneventful, and the preoperative neurological deficits gradually resolved. Histopathologically, the lesion was a schwannoma with intratumoral hemorrhage. Conclusion: This case demonstrates the rare acute presentation of a T12-L1 schwannoma with an accompanying intratumoral hemorrhage resulting in both a SDH/SAH.

Delayed-onset neurological deficit following correction of severe thoracic kyphotic deformity

2008 ◽  
Vol 8 (1) ◽  
pp. 74-79 ◽  
Author(s):  
H. Michael Keyoung ◽  
Adam S. Kanter ◽  
Praveen V. Mummaneni
Keyword(s):  
Neurological Deficit ◽  
Motor Evoked Potentials ◽  
Deformity Correction ◽  
Pedicle Screw Fixation ◽  
Surgical Correction ◽  
Neurological Deficits ◽  
Sensory Loss ◽  
Sensory Level ◽  
Complete Reversal ◽  
Potential Risks

✓There are many potential risks associated with spinal deformity correction procedures including transient and/or permanent neurological deficits. Typically, neurological deficits caused by the surgical correction of spinal kyphosis occur acutely during surgery or immediately after surgery. Delayed postoperative neurological deficits are extremely rare. The authors report a case of delayed neurological deficit that occurred 48 hours after surgical correction of thoracic hyperkyphosis. An 18-year-old man with myotonic dystrophy presented with a 110° T7–L1 kyphosis. The patient underwent an uneventful two-stage correction procedure of the hyperkyphotic deformity. First, anterior discectomies and fusion were performed from T-7 to L-1 using rib autograft, and all segmental vessels were preserved. Subsequently, on the same day, the patient underwent posterior Smith–Petersen osteotomies and T7–L2 pedicle screw fixation. Intact somatosensory and motor evoked potentials were maintained throughout both operations. Postoperatively, he remained neurologically intact without sequelae for nearly 48 hours. On postoperative Day 2, the patient developed delayed monoplegia of the left leg and sensory level loss below T-10. Medical management enabled complete reversal of the patient's monoplegia and sensory loss. At 2-year follow-up, the patient had no adverse neurological sequelae. In this case, a delayed postoperative neurological deficit occurred following spinal hyperkyphosis correction. The authors discuss the possible etiological mechanisms behind this complication and suggest strategies for its management.

Sign in / Sign up

Export Citation Format

Share Document