Tendon Refl Research Articles

КЛИНИЧЕСКИЕ ОСОБЕННОСТИ ОСТРЫХ РЕФЛЕКТОРНЫХ И КОМПРЕССИОННЫХ СИНДРОМОВ ШЕЙНОГО ОСТЕОХОНДРОЗА

Pain syndromes of cervical osteochondrosis are among the most common in neurological practice. The complex anatomic and physiological features of the cervical spine result in a variety of clinical syndromes in case of cervical osteochondrosis. The clinical features of the formation of refl ex and compression syndromes of cervical steochondrosis were identifi ed as a result of the examination. In patients with refl ex pain syndromes, the distribution of pain over the sclerotome and myotome areas (myosclerotome pain)
 and the absence of motor and sensory disorders were characteristic. Patients with compression radicular syndrome featured the distribution of pain sensation over dermatome areas, motor disturbances in the form of muscle paresis or hypotonia, corresponding myotome, decrease or absence of corresponding tendon refl exes, and sensory disturbances in the dermatome area of the aff ected radicle.

Rapid Progression of Extensive Arachnoid Adhesion Longer Than Twelve Segments and Cysts Formation after Posterior Lumbar Interbody Fusion: Case Report

Arachnoid cysts and intradural adhesion are uncommon in postoperative complication rather than congenital condition. The adhesion and cysts are usually around surgical site but some extend to a distant place. The authors report a case of formation of arachnoid cysts and adhesion far away from original surgical site with signifi cant clinical manifestations after posterior lumbar interbody fusion (PLIF).A 55-year-old woman accepted PLIF and got a good recovery but her dura mater was torn and sutured during procedure. Six months after her 1st surgery, she felt rapid progressing numbness from foot to belly and weakness of both lower limbs. On Examination bilateral deep tendon refl exes were hyperactive. Magnetic resonance imaging (MRI) showed intradural adhesion formed from T4 to sacral canal. Cerebrospinal fluid terminated at T4 level and there exactly the arachnoid cyst was formed. The long intradural adhesion and distant cyst formation made this case unique and the cause of neurological manifestations. Then the patient underwent intradural exploratory surgery and cyst-abdominal shunting. The cyst was actually found to be the terminal part of remaining subarachnoid space. Patient’s numbness stopped advancing upward and the strength of both lower limbs gradually improved after surgery. Therefore, arachnoid cyst and adhesion might appear at any place after spine surgery with dural rupture. Exploratory surgery and timely decompression can effectively slow down the progression of disease.Spinal meningeal cysts are rare and have been described as “arachnoid cysts,” “pouches”, or “diverticula”.7 Most spinal intradural arachnoid cysts are thought to be congenital but still some acquired arachnoid cysts were reported as to be the results of trauma, hemorrhage or infection.8 Even fewer were caused by intradural infl ammation after invasive diagnostic test and treatment. Nepal Journal of Neuroscience. Vol. 13, No. 2, 2016, Page: 94-98

A 10-Year-Old Boy with Muscle Cramps

A 10-year-old boy was evaluated for a 4-month history of muscle cramps. Initially, the cramps occurred twice weekly, usually in his calves. More recently, he had been having cramps in both arms and hands which lasted for up to 5 minutes. On occasion, his fi ngers would get “stuck” for several minutes before he could straighten them. Although he still participates in gym class, his mother reported he had become more cautious about physical activity. There was no history of fever, chills, night sweats, weight loss, visual problems, nausea, vomiting, or diarrhea, although in the past year, he also has noted “dark spots” on his ankles and lower extremities. His past history was unremarkable, although his brother has autism with sensory integration problems. On exam, the patient was alert and appeared healthy. Weight and height were in the 50th percentile. Pulse 88, respiratory rate 16, blood pressure 107/61. There were several 2 to 3 cm hyperpigmented patches with irregular borders on his lower extremities. HEENT exam was unremarkable. Lungs were clear. S1 and S2 were normal without murmurs, rubs, or gallops. Abdomen was soft and non-tender without masses or organomegaly. He was Tanner 1. Both testes were descended. Back was straight. Extremities were normal. Muscle mass was normal without tenderness. On neurologic examination, deep tendon refl exes were 2+ bilaterally. Toes were downgoing. Muscle strength was 5/5 throughout. Cranial nerves II through XII were intact. On initial laboratory evaluation, hemoglobin was 9.7 g/dL, white blood cell count 8,600/mm3 with 45% neutrophils, 41% lymphocytes, 10% monocytes; platelet count 178,000 mm3. MCV was 74, MCH 21, RDW 22 (normal 12.5-16), reticulocyte count 4.5%. Chem14 and ionized calcium were normal save for an albumin of 2 g/dL. GGT was normal. Sedimentation rate and C-reactive protein were normal; CPK was 510 IU/L (normal 27-248 IU/L). Robert Listernick, MD, moderator: I know this may be a profound metaphysical, philosophical question, but what’s a muscle cramp? Nancy Kuntz, MD, pediatric neurologist: You couldn’t have picked a topic more sure to create excitement and argument among neuromuscular specialists than, “What are cramps?” and “What does one do about them?” Both clinicians and patients refer to cramps as persistent or continuous unwanted muscle activity beyond what’s functional. The sensation of “getting stuck” is myotonia, in which there’s delay in relaxation of the muscles; the contraction is normal, but muscle membrane abnormalities make it diffi cult for the muscle to relax. Myotonia is uncomfortable, and people complain about pain. In the evaluation of cramps, family history is important, looking for other individuals with cramping, weakness, or who have the sensation of muscles “getting stuck.” What some patients label “cramps” is instead myokymia — localized involuntary muscle quivering — which may be caused by certain drugs or occur as a result of a paraneoplastic process. Finally, sometimes a cramp is just a cramp. Dr. Listernick: Are there clues on exam to the presence of myotonia rather than simple cramps? Dr. Kuntz: One clue is the presence of percussion myotonia. You hit a relaxed muscle with a refl ex Dr. Listernick is professor of pediatrics at Feinberg School of Medicine, Northwestern University, and director of the Diagnostic and Consultation Service, Division of General Academic Pediatrics, Children’s Memorial Hospital, Chicago, IL. fi rm rounds • fi rm rounds • • fi rm rounds • fi rm rounds

A fisherman who could not row

In July, 2007, a 28-year-old man came to our institute. Until recently, he had worked as a fi sherman, off the coast of Kerala—where boats traditionally carry 4–5 fi sher men, who must row against strong currents and waves. He had had to leave his job, because, when rowing, he could not keep to the same rhythm as his fellows: he could not extend his elbows rapidly after fl exion. After 5 min, this problem disappeared. Additionally, he could not release his grip quickly, after holding things tightly. His problems had gradually increased over 5 years; he had had to leave his job, and was now working as an assistant in a roadside shop. He had no other medical history of note. General examination showed nothing of note. Neurological examination showed no abnormality of cognitive function, cranial nerves, the somatosensory system, or cerebellum; power and refl exes were normal, and the patient had no muscle atrophy or fasciculations. However, repeated gripping and releasing of the examiner’s fi ngers, tapping over the extensor digitorum communis, and tapping the tongue revealed grip myotonia, percussion myotonia, and tongue myotonia respectively. Blood tests revealed a high concentration of creatine kinase (CK) (2960 IU/L; normal range 21–232 IU/L). Needle electromyography (EMG) showed diff use myotonic discharges (fi gure), but no evidence of myopathy. On cooling of muscle to 20°C, by wrapping the limb in a plastic bag and immersing it in iced water, and after short and long periods of exercise (voluntary contraction of the muscle tested, for 5–10 s and 3–5 min with brief rest breaks), we found no decrease in compound muscle action-potential amplitude. These fi ndings were consistent with true myotonia. But of what cause? The age of onset, high concentration of CK, and normal EMG after exercise were atypical for myotonia congenita. The persistence of symptoms indicated that the patient probably did not have potassium-aggravated myotonia (also known as myotonia fl uctuans). Slit-lamp examin ation showed no cataract, which, together with the absence of muscle weakness, made type 1 myotonic dystrophy unlikely; moreover, genetic testing for this disease gave a negative result. However, routine echo cardiography revealed mode rate pericardial eff usion without tamponade, so we requested thyroid function tests. The thyrotropin con cen tration was very high (>60 mIU/L; normal range 0∙25–5 mIU/L); tri-iodothyronine and thyroxine concentrations were low, at <0∙4 nmol/L (normal 0∙92–2∙33 nmol/L) and 8∙01 nmol/L (normal 60–120 nmol/L) respect ively. We prescribed thyroxine. The pa tient’s symp toms subsided rapidly. At 3-month and 6-month follow-up, we found no clinical or electro physiological evidence of myotonia; concentrations of CK and thyroid hormones were normal. When last seen, in June, 2008, the patient was well, on a thyroxine dose of 200 μg daily, and had returned to work as a fi sher man. Myotonia is the slow relaxation of muscle, after voluntary contraction or percussion. It is painless, but patients often describe muscle stiff ness that improves with repeated use of muscle, the so-called “warm-up phenomenon”. On examination, myotonia may be evident from a delayed release of the hand, in the introductory handshake. EMG shows spontaneous, repetitive discharges with waxing and waning of amplitude and frequency, producing a characteristic “dive-bomber” like sound. Myotonia can be a presenting sign of myotonic dystrophy; non-dystrophic myotonias, in which mytonia is caused by dysfunction of channels for chloride (in myotonia congenita) or sodium (in paramyotonia congenita, potassium-aggravated myotonia, and hyperkalaemic periodic paralysis with myotonia); myopathies (acid maltase defi ciency, polymyositis, myotubular myopathy); or, rarely, denervation of any cause. Syndromes causing myotonia are distinguished by associated clinical features, and by EMG after cooling and exercise. Pseudomyotonia is slow relaxation without myotonic discharge on EMG, and is found in hypothyroidism, when it is characteristically revealed by testing of tendon refl exes. However, hypothyroidism can also cause true myotonia, and can unmask type 2 myotonic dystrophy. Patients with myotonia caused by hypo thyroidism should be given thyroxine; patients in whom myotonic dystrophy is unmasked may benefi t symptom atically from thyroxine, despite persistent myotonic dis charges on EMG. We suspect, on clinical grounds, that our patient had myotonia caused by hypothyroidism; he declined genetic testing for type 2 myotonic dystrophy.

Chronic cough and Holmes-Adie syndrome

In April, 2006, a 45-year-old white man—a lifelong nonsmoker—was referred to the Royal Brompton Hospital Cough Clinic. In October, 2002, he had presented to his general practitioner with a persistent dry cough. The cough had started in March, 2002, after a bout of pneumonia. In addition, he claimed to have night sweats but no systemic symptoms. Auscultation of his chest, and a chest radiograph were normal, and he had a negative (grade 1) tuberculin skin test. In January, 2003, he was referred to his local chest clinic, where further inves tigations including lung function and CT of the chest were normal. He was reassured and discharged. In June, 2004, he presented to his local eye clinic complaining of blurred vision. Anisocoria was noted with an enlarged tonic left pupil (fi gure) and near light dissociation. Ankle tendon arefl exia was present on the right and elicited on the left only with reinforcement. He was diagnosed with Holmes-Adie syndrome—a condition of unknown cause characterised by tonic pupillary reactions and absent tendon refl exes. In August 2004, he was re-referred back to his local chest clinic because his dry cough persisted. Empirical treatment with omeprazole 20 mg daily was started and he underwent a normal barium swallow. Over the course of the following year, with no improvement in symptoms, he was prescribed an inhaled antimuscarinic bronchodilator (oxitropium bromide), an oral H1-anti histamine (loratadine), and he was given a trial of an H2-receptor antagonist (ranitidine) for 1 month, with no eff ect. When seen by us in April, 2006, his cough had persisted and he reported that during one coughing paroxysm he had experienced syncope. Direct questioning revealed truncal and right arm hyperhydrosis with excessive sweating in the right armpit. Respiratory, nasopharyngeal, and cardiovascular examinations were unremarkable. In particular, the patient had no evidence of dry eyes, dry mouth, or skin changes that might suggest a diagnosis of Sjogren’s syndrome. VDRL, autoantibody screen, and fasting blood sugar were negative. CT of the chest, full lung function (including histamine challenge, nitric oxide, and reversibility testing), nasolaryngo scopy, cinevideo fl uoroscopy, and 24-hour oesophageal pH monitoring were all normal. The patient declined fi breoptic bronchoscopy and capsaicin cough challenge. Treatment with high-dose inhaled corticosteroid (fl uticasone propionate 1000 μg daily) delivered from a pressurised metered-dose inhaler and spacer attachment, induced paroxysms of cough. Two separate courses of high dose oral steroids provided no improvement in either symptomatology or diurnal peak expiratory fl ow rate measurements. The addition of a non-selective oral H1-antihistamine treatment (chlorphenamine maleate 4 mg four times a day) was of no additional benefi t. As of September, 2006, the patient is still symptomatic and awaiting neurological consultation including cardiovascular autonomic testing. Kimber and colleagues, have reported an association between Holmes-Adie syndrome and chronic cough. Our patient showed early signs of autonomic neuropathy as his cough developed, including anisocoria, hyperhydrosis and syncope. The mechanism behind the cough is poorly understood, but it has been proposed that selective loss of thinly myelinated aff erent nerves in the lung, trachea, and larynx leads to denervation hypersensitivity of secondary neurons in the nucleus solitarius. Although the patient undoubtedly had a trigger episode precipitating his chronic cough (the original episode of pneumonia), the presence of an autonomic neuropathy may well explain the persistence of his symptoms. This case also highlights the diffi culty in treating patients with no apparent cause for their cough. Although chronic idiopathic cough and Holmes-Adie syndrome are both of unknown cause, recognition of this association has led to a more accurate diagnosis and, in this case, an appropriate tertiary specialist opinion.