Involuntary Movements Constitute a Group of Neurological Symptoms of Major Significance

Total Page:16

File Type:pdf, Size:1020Kb

Involuntary Movements Constitute a Group of Neurological Symptoms of Major Significance Tohoku J. Exp. Med., 1990, 161, Suppl., 21-27 Involuntary Movements OLAF B. PAULSON Department of Neurology, Rigshospitalet, 9 Blegdamsvej, DK-2100, Copenhagen, Denmark PAULSON, O.B. Involuntary Movements. Tohoku J. Exp. Med., 1990, 161, Suppl., 21-27•\Movements disorders are prominent symptoms in many neur- ological diseases, especially with affection of the basal nuclei. Several of these diseases have characteristic symptoms and signs, whereas clinical diagnosis is more difficult in other diseases. The various movement disorders, hypokinesia, hyper- kinetic syndrome, tremor etc. are defined and described, and clinical features of the various diseases were commented on.•\basal nuclei disease ; dyskinesia ; hyperkinetic syndromes ; hypokinesia ; involuntary movements Involuntary movements constitute a group of neurological symptoms of major significance. For the single patient the movement disorder may be disturbing and disabling. The symptoms are often characteristic leading to an accurate clinical diagnosis. In other instances diagnosis may be difficult. Movement disorders are seen with several neurological diseases, and especially with diseases of the basal nuclei. Comments on the terminology of lesions in the motor system The "classical" terms "pyramidal lesion" and "extrapyramidal lesion" are somewhat incorrect and misleading. Thus, a socalled "pyramidal lesion" with spastic paresis, hypertonia, increased tendon reflexes and extensive plantar response is not due to a pure lesion of the pyramidal tract but to a lesion of a group of pathways running close connection to the classical pyramidal pathway. A pure pyramidal lesion is very uncommon and would in fact give a different picture with facial palsy and extensive plantar response. The so-called "classical pyrami- dal lesion" therefore involves affection of both pyramidal and in its strict sense extrapyramidal structures. The "classical" term "extrapyramidal lesion" has been used synonymous to basal nuclei lesion. This seems not logic since other structures in the motor system could even as well be called extrapyramidal including the cerebellum and the above mentioned motor pathways. The terminology of lesions in the motor system need therefore to be revised. It is proposed that the term supranuclear motor lesion is used for the characteristic lesion of the motor descending (activating) system with symptoms of spastic paresis, increased tendon reflexes and extensive plantar response. The term 21 22 O.B. Paulson infranuclear / nuclear or peripheral lesion will then as ordinarily describe the facial paralysis seen in lesions of the peripheral motor neurons. The uncommon isolated lesion of the pyramidal tract with facial paralysis as mentioned above should be called an isolated lesion of the pyramidal tract itself . A lesion or disease in the basal nuclei should be called a basal nuclei lesion and the term •gextrapyramidal•h should be avoided. A cerebellar lesion is obviously still be called a cerebellar lesion. The anatomical structures in the basal nuclei are the telencephalic structures, the caudate nucleus, globus pallidus, putamen, and claustrum. Globus pallidus and putamen are together called the lentiform nucleus. Although anatomically related the amygelaloid body is here not considered as part of the basal nuclei because it physiologically relates more to the hippocampus and the limbic system. The diencephalic and mesencephalic structures, the subthalamic nucleus and substantia nigra are here considered part of the basal nuclei system since they physiologically are closely connected to the lentiform and caudate nuclei. Many pathways from the basal nuclei goes to the ventrolateral thalamic nucleus which from a physiological point of view also can be considered part of basal nuclei system. TABLE 1. Diseases with movement disorders Involuntary Movements 23 Diseases with movement disorders Several diseases are characterized by or accompanied by movement disorders (Table 1) and many of these affects the basal nuclei. The symptoms and signs seen with diseases of the basal nuclei are listed in Table 2. It appears that movements disorders are the most prominent symptoms in these diseases, and movement disorders are in fact primarily associated with diseases in the basal nuclei. It is characteristic for all movement disorders in basal nuclei diseases that they disappear during sleep and become more marked during emotional stress. Classification, definition and clinical features of movement disorders The different movement disorders are listed in Table 3. Hypokinesia is reduced motor activity. It can have the form of akinesia with reduced spontaneous motor activity despite normal strength and normal coordina- tions, e.g., the patient does not swing the arms when walking. It can also have the form of bradykinesia where all movements are performed solely, at a pathologically reduced velocity, e.g., the patient is extremely slow buttoning a button. Akinesia and bradykinesia is especially characteristic of Parkinson's disease. The hyperkinetic or dyskinetic syndromes characterized by involuntary move- ments can have several forms which often overlaps each other. It is although still advantageous to distinguish between the different syndromes. TABLE2. Symptoms of diseases in the basal nuclei TABLE 3. Movement disorders 24 O.B. Paulson Chorea are variable, irregular, rapid, jerking movements in the extremities or the face. Chorea is often accompanied by hypotonia. Chorea is typically seen in Huntington's chorea. Chorea may be unilateral (hemichorea). If unilateral chorea is especially pronounced in the proximal joints the movement abnormality is called hemiballism. This syndrome is most often due to a vascular lesion in the subthalamic nucleus. Athetosis are somewhat slower, twisting movements. One athetotic move- ment often continues in another. Athetosis is most pronounced in the face and distally in the extremities, and may be provoked if the patient try to keep the face and extremities quite or to perform finer skilled movements. It may not be easy to distinguish chorea and athetosis and chorea and athetosis may occur in the same patient. The term choreoathetosis is then often used. Athetosis is characteristi- cally seen in Huntington's chorea. A special form of athetosis with involuntary movements in the face is characteristic of tardive dyskinesia seen in some patients after many years treatment with neuroleptic drugs. Dystonia or torsion spasms can be described as persisted athetotic movements of the extremities, head or the truncus. It is sometimes induced by drugs and can be seen in Huntington's chorea. Myoclonus are one or a short series of jerks in a muscle group. It can occur with many diseases : In several types of epilepsy, associated with diseases of the basal nuclei, and in some diseases with diffuse affection of the brain such as subacute sclerosing panencephalitis, Creutzfeldt-Jacob's disease and some cases of metabolic encephalopathy. Myoclonus located to the palate and face may be seen with lesions near the fourth ventricle. Myoclonus can also be a quite benign "physiological phenomenon" as seen in sleep myoclonia where a normal person who is half asleep suddenly wakes up due to a myoclonic jerk. Tics are stereotype repetitive involuntary movements in one or a few muscle groups, often in the face or larynx, e.g., a brief cough. The pathogenesis is unknown, but seems often to be of psychogenic nature. In other instances tics accompany diseases affecting the basal nuclei. Gilles de la Tourette syndrome is a special most likely organic disease with tics that may have the character of brief swear-word and which may be most embarrassing for the patient. Other movement disorders, e.g., tremor and seizures are different from the above described irregular involuntary hyperkinetic syndromes. Seizures will not be described here. Tremor is a more or less regular, repeated and often continuous shaking of the head, hands, arms or legs. Tremor may be most marked at rest when relaxed (resting tremor), during static movements such as holding the arms outstretched (static tremor) or when trying to fix an object (intention tremor). Tremor is seen with several diseases and can be categorized in three main groups : One compris- ing the physiological tremor and the somewhat similar essential and thyrotoxic tremor ; one consisting of the cerebellar tremor and one consisting of the parkin- Involuntary Movements 25 sonian tremor. Physiologic tremor is of low amplitude and rather high frequency (8-12 cps). It occurs often at rest and may be aggravated by movements. Normally physiological tremor is absent, but may be provoked by extreme fatigue , in stress situations with activation of the sympathetic nervous system, and in all individuals following intravenous injection of epinephrine. Shivering may be considered as a special type of physiological tremor. Essential tremor is often familial and a little slower than the physiological. It is provoked by movements and characteristically the tremor most often disappears following the ingestion of a small amount of alcohol. Thyrotoxic tremor resembles the physiological, but is somewhat faster. Cerebellar tremor is especially pronounced with lesion of the dentate nucleus, of the other cerebellar roof nucleus or of the pathways through the superior cerebellar peduncle from these nuclei to the red nucleus in the mesencephalon. This type of cerebellar tremor is characterized by a crescendo like marked increase of its amplitude when the patient
Recommended publications
  • Physiology of Basal Ganglia Disorders: an Overview
    LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES SILVERSIDES LECTURE Physiology of Basal Ganglia Disorders: An Overview Mark Hallett ABSTRACT: The pathophysiology of the movement disorders arising from basal ganglia disorders has been uncer­ tain, in part because of a lack of a good theory of how the basal ganglia contribute to normal voluntary movement. An hypothesis for basal ganglia function is proposed here based on recent advances in anatomy and physiology. Briefly, the model proposes that the purpose of the basal ganglia circuits is to select and inhibit specific motor synergies to carry out a desired action. The direct pathway is to select and the indirect pathway is to inhibit these synergies. The clinical and physiological features of Parkinson's disease, L-DOPA dyskinesias, Huntington's disease, dystonia and tic are reviewed. An explanation of these features is put forward based upon the model. RESUME: La physiologie des affections du noyau lenticulaire, du noyau caude, de I'avant-mur et du noyau amygdalien. La pathophysiologie des desordres du mouvement resultant d'affections du noyau lenticulaire, du noyau caude, de l'avant-mur et du noyau amygdalien est demeuree incertaine, en partie parce qu'il n'existe pas de bonne theorie expliquant le role de ces structures anatomiques dans le controle du mouvement volontaire normal. Nous proposons ici une hypothese sur leur fonction basee sur des progres recents en anatomie et en physiologie. En resume, le modele pro­ pose que leurs circuits ont pour fonction de selectionner et d'inhiber des synergies motrices specifiques pour ex£cuter Taction desiree. La voie directe est de selectionner et la voie indirecte est d'inhiber ces synergies.
    [Show full text]
  • New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting As Intractable Oromandibular Dystonia
    Freely available online New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting as Intractable Oromandibular Dystonia 1,2 2,3 1,3* Kyung Ah Woo , Jee-Young Lee & Beomseok Jeon 1 Department of Neurology, Seoul National University Hospital, Seoul, KR, 2 Department of Neurology, Seoul National University Boramae Hospital, Seoul, KR, 3 Seoul National University College of Medicine, Seoul, KR Keywords: Dystonia, spinocerebellar ataxia type 2, Parkinson’s disease Citation: Woo KA, Lee JY, Jeon B. Familial spinocerebellar ataxia type 2 parkinsonism presenting as intractable oromandibular dystonia. Tremor Other Hyperkinet Mov. 2019; 9. doi: 10.7916/D8087PB6 * To whom correspondence should be addressed. E-mail: [email protected] Editor: Elan D. Louis, Yale University, USA Received: October 20, 2018 Accepted: December 10, 2018 Published: February 21, 2019 Copyright: ’ 2019 Woo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution–Noncommercial–No Derivatives License, which permits the user to copy, distribute, and transmit the work provided that the original authors and source are credited; that no commercial use is made of the work; and that the work is not altered or transformed. Funding: None. Financial Disclosures: None. Conflicts of Interest: The authors report no conflict of interest. Ethics Statement: This study was reviewed by the authors’ institutional ethics committee and was considered exempted from further review. We have previously described a Korean family afflicted with reflex, mildly stooped posture, and parkinsonian gait. There was spinocerebellar ataxia type 2 (SCA2) parkinsonism in which genetic no sign of lower motor lesion, including weakness, muscle atrophy, analysis revealed CAG expansion of 40 repeats in the ATXN2 gene.1 or fasciculation.
    [Show full text]
  • Cramp Fasciculation Syndrome: a Peripheral Nerve Hyperexcitability Disorder Bhojo A
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by eCommons@AKU Pakistan Journal of Neurological Sciences (PJNS) Volume 9 | Issue 3 Article 7 7-2014 Cramp fasciculation syndrome: a peripheral nerve hyperexcitability disorder Bhojo A. Khealani Aga Khan University Hospital, Follow this and additional works at: http://ecommons.aku.edu/pjns Part of the Neurology Commons Recommended Citation Khealani, Bhojo A. (2014) "Cramp fasciculation syndrome: a peripheral nerve hyperexcitability disorder," Pakistan Journal of Neurological Sciences (PJNS): Vol. 9: Iss. 3, Article 7. Available at: http://ecommons.aku.edu/pjns/vol9/iss3/7 CASE REPORT CRAMP FASCICULATION SYNDROME: A PERIPHERAL NERVE HYPEREXCITABILITY DISORDER Bhojo A. Khealani Assistant professor, Neurology section, Aga khan University, Karachi Correspondence to: Bhojo A Khealani, Department of Medicine (Neurology), Aga Khan University, Karachi. Email: [email protected] Date of submission: June 28, 2014, Date of revision: August 5, 2014, Date of acceptance:September 1, 2014 ABSTRACT Cramp fasciculation syndrome is mildest among all the peripheral nerve hyperexcitability disorders, which typically presents with cramps, body ache and fasciculations. The diagnosis is based on clinical grounds supported by electrodi- agnostic study. We report a case of young male with two months’ history of body ache, rippling, movements over calves and other body parts, and occasional cramps. His metabolic workup was suggestive of impaired fasting glucose, radio- logic work up (chest X-ray and ultrasound abdomen) was normal, and electrodiagnostic study was significant for fascicu- lation and myokymic discharges. He was started on pregablin and analgesics. To the best of our knowledge this is report first of cramp fasciculation syndrome from Pakistan.
    [Show full text]
  • Drug-Induced Movement Disorders
    Expert Opinion on Drug Safety ISSN: 1474-0338 (Print) 1744-764X (Online) Journal homepage: https://www.tandfonline.com/loi/ieds20 Drug-induced movement disorders Dénes Zádori, Gábor Veres, Levente Szalárdy, Péter Klivényi & László Vécsei To cite this article: Dénes Zádori, Gábor Veres, Levente Szalárdy, Péter Klivényi & László Vécsei (2015) Drug-induced movement disorders, Expert Opinion on Drug Safety, 14:6, 877-890, DOI: 10.1517/14740338.2015.1032244 To link to this article: https://doi.org/10.1517/14740338.2015.1032244 Published online: 16 May 2015. Submit your article to this journal Article views: 544 View Crossmark data Citing articles: 4 View citing articles Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=ieds20 Review Drug-induced movement disorders Denes Za´dori, Ga´bor Veres, Levente Szala´rdy, Peter Klivenyi & † 1. Introduction La´szlo´ Vecsei † University of Szeged, Albert Szent-Gyorgyi€ Clinical Center, Department of Neurology, Faculty of 2. Methods Medicine, Szeged, Hungary 3. Drug-induced movement disorders Introduction: Drug-induced movement disorders (DIMDs) can be elicited by 4. Conclusions several kinds of pharmaceutical agents. The major groups of offending drugs include antidepressants, antipsychotics, antiepileptics, antimicrobials, antiar- 5. Expert opinion rhythmics, mood stabilisers and gastrointestinal drugs among others. Areas covered: This paper reviews literature covering each movement disor- der induced by commercially available pharmaceuticals. Considering the mag- nitude of the topic, only the most prominent examples of offending agents were reported in each paragraph paying a special attention to the brief description of the pathomechanism and therapeutic options if available. Expert opinion: As the treatment of some DIMDs is quite challenging, a pre- ventive approach is preferable.
    [Show full text]
  • Deformities of the Hands and Feet in Parkinsonism and Their Reversibility by Operation
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.26.1.33 on 1 February 1963. Downloaded from J. Neurol. Neurosurg. Psychiat., 1963, 26, 33 Deformities of the hands and feet in Parkinsonism and their reversibility by operation PETER GORTVAI From the National Hospital for Nervous Diseases, Queen Square, London Charcot (1877) described some aspects of the typical method using a small instrument which screws deformities of the hands and feet seen in Parkinson's directly into the skull and depends on localization disease. He likened the deformity of the hands to that of the target in the brain on the measurement of sometimes observed in chronic progressive rheu- angles in two planes. The lesions in the ventrolateral matism. He said that the differential diagnosis is nucleus of the thalamus were made by the injection usually made with ease, because in cases of Parkin- of 0 5 to 1 ml. of a mixture of Etopalin (Ciba) and sonism 'there is found neither the articular tume- kaolin. faction and stiffness, nor the osseous deposits and cracking sounds observed in nodose rheumatism'. DESCRIPTION OF THE DEFORMITIES guest. Protected by copyright. He describes the deformity of the toes as a 'griffe' (or claw), on account of the extension of the first and THE HANDS In its early and commonest stage the concomitant flexion of the second phalanges. deformity amounts to no more than a characteristic Hughlings Jackson (1899) also mentions deformity posture of the affected hand (Fig. 1). The fingers are of hands seen in some cases of Parkinsonism. He held extended at the interphalangeal joints and remarked that 'in paralysis agitans the interossei are flexed some 40° to 700 at the metacarpo-phalangeal the muscles of the hand which are preponderatingly joints.
    [Show full text]
  • Nocturnal Leg Cramps: Is There Any Relief?
    Nocturnal leg cramps: is there any relief? Nocturnal leg cramps are common, particularly in older people and in women who are pregnant. The condition is characterised by painful cramps in the legs or feet, that affect sleep quality. Is there an effective treatment? Unfortunately, treatment options are limited, but lifestyle modifications and gentle stretching may have some effect. Pharmacological treatment may be considered for people with frequent, severe leg cramps, however, quinine is no longer recommended. What are nocturnal leg cramps? Factors known to be associated with an increased risk of nocturnal cramping, include:1 A nocturnal leg cramp is a sudden contraction of muscles in the leg or foot during sleep. This painful tightening of the Age over 50 years muscle can last from a few seconds to several minutes. Cramps Pregnancy often cause waking, and although the cramps themselves are Exercise, particularly over-exertion benign, the affected muscle may be painful for some hours Leg positioning, e.g. prolonged sitting with legs afterwards and the consequences of sleep impairment can be crossed, tight bed covers which cause the toes to point considerable. downwards Excessive consumption of alcohol Severe nocturnal cramps are characterised by painful, incapacitating episodes, which last on average for nine Chronic dehydration minutes, and recur intermittently throughout the night.1 Structural disorders, e.g. flat feet or other foot and ankle This can lead to secondary insomnia and impaired day-time malformations functioning. Approximately 20% of people who experience Medicines, e.g. diuretics (especially thiazide and regular nocturnal cramps have symptoms severe enough to potassium-sparing diuretics), some anti-inflammatories affect sleep quality or require medical attention.1 (e.g.
    [Show full text]
  • Radiologic-Clinical Correlation Hemiballismus
    Radiologic-Clinical Correlation Hemiballismus James M. Provenzale and Michael A. Schwarzschild From the Departments of Radiology (J.M.P.), Duke University Medical Center, Durham, and f'leurology (M.A.S.), Massachusetts General Hospital, Boston Clinical History derived from the Greek word meaning "to A 65-year-old recently retired surgeon in throw," because the typical involuntary good health developed disinhibited behavior movements of the affected limbs resemble over the course of a few months, followed by the motions of throwing ( 1) . Such move­ onset of unintentional, forceful flinging move­ ments usually involve one side of the body ments of his right arm and leg. Magnetic res­ (hemiballismus) but may involve one ex­ onance imaging demonstrated a 1-cm rim­ tremity (monoballism), both legs (parabal­ enhancing mass in the left subthalamic lism), or all the extremities (biballism) (2, 3). region, which was of high signal intensity on The motions are centered around the shoul­ T2-weighted images (Figs 1A-E). Positive der and hip joints and have a forceful, flinging serum human immunodeficiency virus anti­ quality. Usually either the arm or the leg is gen and antibody titers were found, with predominantly involved. Although at least mildly elevated cerebrospinal fluid toxo­ some volitional control over the affected plasma titers. Anti-toxoplasmosis treatment limbs is still maintained, the involuntary with sulfadiazine and pyrimethamine was be­ movements typically can be checked by the gun, with resolution of the hemiballistic patient for only a few moments ( 1). The movements within a few weeks and decrease movements are usually continuous but may in size of the lesion.
    [Show full text]
  • Limb Dystonia Including Writer's Cramp
    Limb dystonia including writer’s cramp Limb dystonia can occur in primary dystonias or as a complication in neurodegenerative diseases e.g. Huntington’s disease, Wilson’s disease or Parkinson syndromes or other diseases like structural brain damage, peripheral trauma or drug-induced. Any muscle group under voluntary control can be affected, dystonic muscle overactivity can occur during rest, be aggravated by movement, or occur only during voluntary movement (action dystonia). If the dystonia is triggered by a specific task, it is called “task-specific” dystonia and affects mostly the hand. As task-specific dystonia causes most disability and is the greatest therapeutic challenge, this summary will focus mainly on this form of limb dystonia. Exercises with a repetitive movement pattern such as writing, typing or playing musical instruments are predestinated to this type of dystonia (1). Co-contraction of agonist and antagonist muscles lead to abnormal postures and movements sometimes associated with tremor or myoclonic jerks. This leads to disability in occupations with repetitive fine motor tasks. The underlying pathophysiology why some individuals develop such a task-specific dystonia and others not, despite of maybe excessive overuse of the hand remains unclear. Safety and efficacy of botulinum toxin has been well established during decades of use (2). Pathophysiology Numerous studies in task-specific dystonias have shown abnormalities within the basal ganglia and its circuits, decreased inhibition at various levels of the sensorimotor system, abnormal plasticity and impaired sensorimotor processing (3). MRI- based volumetric techniques have shown changes in the basal ganglia, thalamus and gray matter of the sensorimotor cortex (4).
    [Show full text]
  • Movement Disorders in Metabolic Disorders
    Current Neurology and Neuroscience Reports (2019) 19: 7 https://doi.org/10.1007/s11910-019-0921-3 NEUROLOGY OF SYSTEMIC DISEASES (J BILLER, SECTION EDITOR) Movement Disorders in Metabolic Disorders José Luiz Pedroso1 & Orlando G. Barsottini1 & Alberto J. Espay2 Published online: 9 February 2019 # Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Purpose of Review We provide a review of the movement disorders that complicate selected metabolic disorders, including the abnormal movements that may appear during or after their treatment. Recent Findings Movement disorders may be underrecognized when arising in the context of a broad range of metabolic disorders. Summary Abnormal movements may occur as the initial manifestation of a systemic disease, at any time during its course, or as a result of the medical interventions required for its management. Ascertaining movement phenome- nology in acute and subacute presentations may assist in the determination of the specific underlying metabolic disorder. The management of movement disorders associated with metabolic disorders depends on the underlying pathophysiology. Keywords Movement disorders . Abnormal movements . Metabolic disorders . Electrolytes . Internal medicine Introduction such as disorders of consciousness, headache, and sei- zures [3]. The metabolic origin can also be suspected Movement disorders such as parkinsonism, tremor, dys- when movement abnormalities appear in emergency set- tonia, chorea, and myoclonus most often arise in several tings or in intensive care units [4]. neurodegenerative or structural diseases of the basal Some common metabolic disorders, such as organ ganglia [1]. They may also be part of the clinical man- failure (particularly liver or renal insufficiency), endocri- ifestations of systemic metabolic disorders, as the initial nological diseases (e.g., hyperglycemia), and electrolyte feature, complicating its course, or as a result of the disturbances, are frequently present with neurological corrective treatment [2•].
    [Show full text]
  • Myelopathy—Paresis and Paralysis in Cats
    Myelopathy—Paresis and Paralysis in Cats (Disorder of the Spinal Cord Leading to Weakness and Paralysis in Cats) Basics OVERVIEW • “Myelopathy”—any disorder or disease affecting the spinal cord; a myelopathy can cause weakness or partial paralysis (known as “paresis”) or complete loss of voluntary movements (known as “paralysis”) • Paresis or paralysis may affect all four limbs (known as “tetraparesis” or “tetraplegia,” respectively), may affect only the rear legs (known as “paraparesis” or “paraplegia,” respectively), the front and rear leg on the same side (known as “hemiparesis” or “hemiplegia,” respectively) or only one limb (known as “monoparesis” or “monoplegia,” respectively) • Paresis and paralysis also can be caused by disorders of the nerves and/or muscles to the legs (known as “peripheral neuromuscular disorders”) • The spine is composed of multiple bones with disks (intervertebral disks) located in between adjacent bones (vertebrae); the disks act as shock absorbers and allow movement of the spine; the vertebrae are named according to their location—cervical vertebrae are located in the neck and are numbered as cervical vertebrae one through seven or C1–C7; thoracic vertebrae are located from the area of the shoulders to the end of the ribs and are numbered as thoracic vertebrae one through thirteen or T1–T13; lumbar vertebrae start at the end of the ribs and continue to the pelvis and are numbered as lumbar vertebrae one through seven or L1–L7; the remaining vertebrae are the sacral and coccygeal (tail) vertebrae • The brain
    [Show full text]
  • Physiotherapy of Focal Dystonia: a Physiotherapists Personal Experience
    European Journal of Neurology 2010, 17 (Suppl. 1): 107–112 doi:10.1111/j.1468-1331.2010.03061.x Physiotherapy of focal dystonia: a physiotherapistÕs personal experience J.-P. Bleton Universite´ Paris Descartes INSERM U894, Service de Neurologie, Hoˆpital Sainte-Anne, Paris, France Keywords: The approach of the physiotherapist to each form of dystonia is individual and has to dystonia, physiotherapy, be specific. There is not one single method but several strategies related to the different cervical dystonia, writerÕs clinical forms. Although there is no standard programme applicable to all forms of cramp, writing tremor, cervical dystonia, we can distinguish a number of guidelines for the different clinical relaxation, pen grip forms. In the myoclonic form, emphasis is placed on seeking to immobilize the head, training and for the tonic form, on rehabilitating corrector muscles. Physiotherapy and bot- ulinum toxin injections mutually interact in order to reduce the symptoms. Recent Received 3 August 2009 studies have shown the clinical benefits of physiotherapy. The physiotherapy of wri- Accepted 5 March 2010 terÕs cramp is designed as a re-learning process. The first step is to perform exercises to improve independence and precision of fingers and wrist movements. Then, the muscles involved in the correction of dystonic postures are trained by drawing loops, curves and arabesques. The aim of rehabilitation is not to enable patients with writerÕs cramp to write as they used to, but to help their dysgraphia evolve towards a fast, fluid and effortless handwriting. A reshaping of the sensory cortical hand representation appears to be associated with clinical improvement in patients with dystonia after rehabilitation.
    [Show full text]
  • Hypocalcaemic Tetany After Total Thyroidectomy Original Article
    Faridpur Med. Coll. J. 2015;10(2):59-62 Original Article Hypocalcaemic Tetany After Total Thyroidectomy NN Biswas1, WA Chaudhury2, JA Khan3, AC Biswas4, KM Arif5, S Ghosh6, S Akter7 Abstract: Hypocalcaemic tetany is one the commonest complication after total thyroidectomy. It may cause significant morbidity. Early detection and treatment have better out come. The main objective of the study is to find the incidence of hypcalcaemic tetany in post operative period after total thyroidectomy and average interval period of hypocalcaemia following surgery. This was an observational study conducted in the department of Otolaryngology & head-Neck Surgery Sylhet M.A.G. Osmani Medical College Hospital during 1st January 2006 to 31st December 2007. Pre-operative routine investigation, Thyroid Function test, Ultrasonography thyroid gland and cytological evaluation by FNAC were done in all patients. Ten patient developed hypocalcaemia after surgery. Among them only one suffered from permanent hypocalcaemia. Most of the patient developed symptoms about 48 hours after surgery. The Incidence and time interval of development of hypocalcaemic tetany after total thyroidectomy found in the series fully coincides with the results of other researchers globally. Key words: Tetany, Total Thyroidectomy, Hypocalcaemic. Introduction: Total thyroidectomy is a logical treatment for patients with thyroid disease in whom the pathologic process Calcium is the sedater of nerve. It is the free, ionized involves both lobes of the thyroid or difficult is a calcium in the body fluids that is necessary for nerve significant consideration as in benign multinodular conduction, muscle contraction and blood coagulation. A goitre, Grave's disease and cancer. Meticulous and decrease in extracellular Ca++ exerts a net excitatory clean cut identification of parathyroid with its effect on nerve and muscle cells.
    [Show full text]