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Practical Neurology 2005; 5: 210–217 Cross References Flick sign; Phalen’s sign; Tinel’s sign Closing-In Sign Copying of drawings which are close to treatment walking pneumonia buy 300 mg combivir otc or superimposed on the original has been referred to symptoms concussion buy combivir online now as the ‘closing-in’ sign treatment for 6mm kidney stone proven combivir 300 mg. It may be seen in patients with Alzheimer’s disease with de cits in visuospatial function symptoms 39 weeks pregnant discount 300mg combivir with visa. Mechanism of the closing-in phenomenon in a gure copying task in Alzheimer’s disease patients. Cluster Breathing Damage at the pontomedullary junction may result in a breathing pattern char acterized by a cluster of breaths following one another in an irregular sequence. Cross Reference Coma Coactivation Sign this sign is said to be characteristic of psychogenic tremors, namely, increased tremor amplitude with loading (cf. These phenomena are said to be characteristic signs of ocular myasthenia gravis and were found in 60% of myasthenics in one study. They may also occur occasionally in other oculomotor brainstem disorders such as Miller Fisher syndrome, but are not seen in normals. Cogan’s lid twitch sign should not be confused with either Cogan’s syn drome, an autoimmune disorder of episodic vertigo, tinnitus, hearing loss, and interstitial keratitis; or the oculomotor apraxia of Cogan, a congenital lack of lateral gaze. Myasthenia gravis: a review of the disease and a description of lid twitch as a characteristic sign. A prospective study assessing the utility of Cogan’s lid twitch sign in patients with isolated unilateral or bilateral ptosis. Collapsing Weakness Collapsing weakness, or ‘give-way’ weakness, suggesting intermittent voluntary effort, is often taken as a sign of functional weakness. Although sometimes labelled as ‘volitional weakness’, it is not clear that such weakness is in any con scious sense willed, and it is therefore probably better to use a non-committal -87 C Collier’s Sign term such as ‘apparent weakness’. Such collapsing weakness has also been recorded following acute brain lesions such as stroke. Cross References Functional weakness and sensory disturbance; Spasticity; Weakness; ‘Wrestler’s sign’ Collier’s Sign Collier’s sign (‘posterior fossa stare’, ‘tucked lid’ sign), rst described in 1927, is elevation and retraction of the upper eyelids, baring the sclera above the cornea, with the eyes in the primary position or looking upward. There may be accompanying paralysis of vertical gaze (especially upgaze) and light-near pupillary dissociation. The sign is thought to re ect damage to the posterior commissure levator inhibitory bres. Nuclear ophthalmoplegia with special reference to retraction of the lids and ptosis and to lesions of the posterior commissure. It represents a greater degree of impairment of consciousness than stupor or obtundation, all three forming part of a continuum, rather than discrete stages, ranging from alert to comatose. This lack of precision prompts some authorities to prefer the description of the individual aspects of neurological function in unconscious patients, such as eye movements, limb movements, vocalization, and response to stimuli, since this conveys more information than the use of terms such as coma, stupor, or obtundation, or the use of a lumped ‘score’, such as the Glasgow Coma Scale. Assessment of the depth of coma may be made by observing changes in eye move ments and response to central noxious stimuli: roving eye movements are lost before oculocephalic responses; caloric responses are last to go. Unrousability which results from psychiatric disease, or which is being feigned (‘pseudocoma’), also needs to be differentiated. A number of neurobehavioural states may be mistaken for coma, including abulia, akinetic mutism, catatonia, and the locked-in syndrome. Cross References Abulia; Akinetic mutism; Caloric testing; Catatonia; Decerebrate rigid ity; Decorticate rigidity; Locked-in syndrome; Obtundation; Oculocephalic response; Roving eye movements; Stupor; Vegetative states; Vestibulo-ocular re exes Compulsive Grasping Hand this name has been given to involuntary left-hand grasping related to all right-hand movements in a patient with a callosal haemorrhage. This has been interpreted as a motor grasp response to contralateral hand movements and a variant of anarchic or alien hand. The description does seem to differ from that of behaviours labelled as forced groping and the alien grasp re ex. In its ‘pure’ form, there is a dissociation between relatively preserved auditory and reading com prehension of language and impaired repetition (in which the phenomenon of conduit d’approche may occur) and naming. Reading comprehension is good or normal and is better than reading aloud which is impaired by paraphasic errors. Conduction aphasia was traditionally explained as due to a disconnection between sensory (Wernicke) and motor (Broca) areas for language, involving the arcuate fasciculus in the supramarginal gyrus. Certainly the brain damage (usu ally infarction) associated with conduction aphasia most commonly involves the left parietal lobe (lower postcentral and supramarginal gyri) and the insula, but it is variable, and the cortical injury may be responsible for the clinical picture. Conduction aphasia is most often seen during recovery from Wernicke’s aphasia, and clinically there is often evidence of some impairment of compre hension. Cross References Anomia; Aphasia; Broca’s aphasia; Conduit d’approche; Paraphasia; Transcortical aphasias; Wernicke’s aphasia Conduit d’approche Conduit d’approche, or ‘homing-in’ behaviour, is a verbal output phenomenon applied to patients with conduction aphasia attempting to repeat a target word, in which multiple phonemic approximations of the word are presented, with gradual improvement until the target word is achieved. This phenomenon sug gests that an acoustic image of the target word is preserved in this condition. A similar phenomenon may be observed in patients with optic aphasia attempting to name a visual stimulus. A similar behaviour is seen in so-called speech apraxia, in which patients repeatedly approximate to the desired output before reaching it. The term may also be used to refer to a parapraxis in which patients attempt to perform a movement several times before achieving the correct movement. Cross References Aphasia; Conduction aphasia; Optic aphasia; Parapraxia, Parapraxis; Speech apraxia 90 Congenital Nystagmus C Confabulation the old de nition of confabulation as the falsi cation of episodic mem ory occurring in clear consciousness, often in association with amnesia (in other words, paramnesias related as true events), has proven increasingly de cient, not least because most amnesic patients, suffering from medial temporal lobe/hippocampal lesions, do not confabulate, and poor memory alone cannot explain confabulation. Schnider has developed a fourfold schema of intrusions, momentary confabulations, fantastic confabulations, and behaviourally sponta neous confabulations, of which the latter are clinically the most challenging. Anterior limbic structures are thought culpable, and the pathogenesis includes a wide variety of diseases, which may include associated phenomena such as amnesia, disorientation, false recognition syndromes including the Capgras delu sion, and anosognosia. Psychophysical and neuroimaging studies suggest that confabulators have reality confusion and a failure to integrate contradictory information due to the failure of a ltering process, 200–300 ms after stimulus presentation and before recognition and re-encoding, which normally permits suppression of currently irrelevant memories. Cross References Amnesia; Asomatognosia; Cortical blindness; Delusion; Paramnesia Confusion Confusion, understood as the inability to think with one’s customary clarity and coherence, is a feature of not only delirium, but also of other situations (encephalopathies, attentional disorders). Moreover, as there is a lack of corre lation of meaning when this term is used by different health professionals, it is regarded by some as an unhelpful term. Cross Reference Delirium Congenital Nystagmus Congenital nystagmus is a pendular nystagmus with the following characteristics: • Usually noted at birth or in early infancy; sometimes may only become apparent in adult life; • Irregular waveforms; • Conjugate; • Almost always horizontal; -91 C Consensual Light Re ex • Accentuated by xation, attention, anxiety; • Decreased by convergence, active eyelid closure; • Often a null point or region; • No complaint of oscillopsia; • It may appear with blindness of childhood onset. Acquired pendular nystagmus may be a result of neurological disease which may present in childhood, such as Pelizaeus–Merzbacher disease, mitochondrial disease, multiple sclerosis, and Whipple’s disease. This may be due to a variety of factors, including prolonged muscle spasticity with or without muscle brosis. This often occurs in the context of limb immobilization or inactivity, for example, in a exed posture. Injections of botulinum toxin to abolish muscle spasticity may be required to assess whether there is concurrent ligamentous restriction, and thus to plan opti mum treatment, which may involve surgery. This may be • Vocal: involuntary utterance of obscenities; • Mental: compulsion to think obscenities. The former is a complex vocal tic most characteristically seen in Tourette syndrome although it actually occurs in less than half of affected individuals. Other recognized disease associations are as follows: • Lesch–Nyhan syndrome; • Postencephalitic parkinsonism; • Neuroacanthocytosis; • Cingulate cortical seizures. The pathophysiology of coprolalia is unknown but may be related to frontal (cingulate and orbitofrontal) dysfunction, for which there is some evidence in Tourette syndrome. Cross Reference Tic Copropraxia Copropraxia is a complex motor tic comprising obscene gesturing, sometimes seen in Tourette syndrome. Cross References Coprolalia; Tic Corectopia Corectopia is pupillary displacement, which may be seen with midbrain lesions, including transtentorial herniation and top-of-the-basilar syndrome, peripheral oculomotor nerve palsies, and focal pathology in the iris. Corneal Re ex the corneal re ex consists of a bilateral blink response elicited by touching the cornea lightly, for example, with a piece of cotton wool. As well as observing whether the patient blinks, the examiner should also ask whether the stimulus was felt: a difference in corneal sensitivity may be the earliest abnormality in this re ex. The bres subserving -93 C Corneomandibular Re ex the corneal re ex seem to be the most sensitive to trigeminal nerve compression or distortion: an intact corneal re ex with a complaint of facial numbness leads to suspicion of a non-organic cause. Trigeminal nerve lesions cause both ipsilateral and contralateral corneal re ex loss. Cerebral hemisphere (but not thalamic) lesions causing hemiparesis and hemisensory loss may also be associated with a decreased corneal re ex. The corneal re ex has a high threshold in comatose patients and is usually preserved until late (unless coma is due to drug overdose), in which case its loss is a poor prognostic sign. Cross References Blink re ex; Coma; Cerebellopontine angle syndrome; Corneomandibular re ex; Facial paresis Corneomandibular Re ex the corneomandibular re ex, also known as the corneopterygoid re ex or Wartenberg’s re ex or sign, consists of anterolateral jaw movement following corneal stimulation. Cortical blindness may result from: • Bilateral (sequential or simultaneous) posterior cerebral artery occlusion; • ‘Top of the basilar syndrome’; • Migraine; • Cerebral anoxia; 94 Coup de Sabre C • Bacterial endocarditis; • Wegener’s granulomatosis; • Following coronary or cerebral angiography (may be transient); • Epilepsy (transient); • Ciclosporin therapy. Patients with cortical blindness may deny their visual defect (Anton’s syn drome, visual anosognosia) and may confabulate about what they ‘see’. Cross References Anosognosia; Confabulation; Macula sparing, Macula splitting; Optokinetic nystagmus, Optokinetic response; Prosopagnosia; Pupillary re exes; Visual agnosia Cotard’s Syndrome A delusional syndrome, rst described in the 1890s, characterized by the patient’s denial of their own existence, or of part of their body.

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Signs and Symptoms: When this muscle is tight medicine stick order combivir now, the horse shows pronounced soreness over the withers medications heart disease cheap combivir 300mg mastercard. During movement medicine information discount 300mg combivir mastercard, the animal resists the downward movement of his head and lateral movement to medications questions discount combivir 300 mg with amex the side opposite the tightness. If the stress point is very Body Parts and Their Stress Points 207 tender the horse will flinch, and perhaps try to pull away from the pressure. It is located on the insertion tendon of the spinalis dorsi muscle, along the crest of the withers at the level of the ninth thoracic vertebra. Both muscles draw the scapula upwards and either forwards or backwards, depending on the action in play. The cervical part of the trapezius pulls the scapula forward and the thoracic part of the trapezius pulls the scapula backward. Signs and Symptoms: When the muscles are tight, the horse reacts to the tightening of the girth. When in action, the animal loses flexibility in his shoulder movement, which results in reduced motion, poor coordination, and loss of power from the foreleg. All this will trigger other compensating stress points among other muscle groups, both in the shoulder and in the hindquarters. If the stress point is very tender, the horse will flinch, perhaps trying to pull away from the pressure. Stress points 6, 7 and 8 will be felt as tight lines running from withers to scapula, which will feel very tender to the horse. The supraspinatus and infraspinatus muscles play a very important role 208 Equine Massage in prevention of lateral dislocation of the shoulder joint. Any lat eral work (for example, side pass) will put stress on these two mus cles. When contracting, the supraspinatus muscle extends the shoulder joint as well as prevents lateral dislocation. Signs and Symptoms: When this muscle is tight, the horse will hold the leg bent at the knee (flexed) due to the referred pain (the occurrence of pain in an area of the body compensating for an injury or soreness in a corresponding portion of the body) into the shoulder joint. The referred pain affects the shoulder joint because the supraspinatus lower tendon attaches in the fascia that surrounds the shoulder joint. During movement, this tight ness causes lameness in the shoulder, resulting in abnormal stride of the foreleg in all planes, therefore affecting the horse’s gait. This is a sign of excessive tight ness and stress; if you feel heat, suspect inflammation. Stress point 9 will be felt as a large, tight knot in the upper end of the muscle. The infraspinatus and supraspinatus muscles play a very important role in prevention of lateral dislocation of the shoulder joint. When contracting, these muscles flex the shoulder joint as well as prevent lateral dislocation. Signs and Symptoms: When the muscles are tight, the horse will hold his leg bent (flexed) at the knee as a result of the referred pain in the shoulder joint. The referred pain affects the shoulder joint because the infraspinatus lower tendon attaches in the fascia that surrounds the shoulder joint. So when this muscle aches the soreness spreads right over the joint capsule fascia. Body Parts and Their Stress Points 209 During movement, the stress causes lameness in the overall shoulder motion, resulting in abnormal stride of the foreleg in all planes and affecting the general gait. Stress point 10 will be felt as a large, tight knot in the upper end of the muscle. When contracting, it moves the scapula back wards, allowing the shoulder joint to come up. Signs and Symptoms: When the muscle is tight, the horse reacts to the tightening of the girth. The stride will be stilted on that side (especially when the girth is tight), interfer ing with the flexibility of the shoulder. This is a sign of excessive tightness and stress; if you feel heat, suspect inflam mation. Stress point 11 will be felt as a large, tight knot by the upper posterior edge of the scapula. It runs down on each side to attach on the upper medial aspect of the humerus of the foreleg. Its contraction is one of the main sources of power for the retraction of the foreleg. The stride will be shortened on that side and the retraction power will be reduced. Stress point 12 will be felt as a large, tight knot by the lower aspect of the muscle near the edge of the triceps muscle. The whole muscle might feel tight along its course, depending on the severity of the stress. Signs and Symptoms: When the muscle is tight, the horse will hold his leg bent (flexed) and will not put weight on it while at rest. During action, the horse will show lameness with a shortened stride; he will jump flat or hang a leg. If the stress point is very tender, the horse will flinch and perhaps stamp his feet on the same side or try to pull away from the pressure. Stress point 13 will be felt as a small knot against the middle posterior edge of the scapula, which may be very tender to the horse. Body Parts and Their Stress Points 211 #14 Stress Point—The Lower End of the Triceps Muscle Myology: the triceps muscle (located in the superficial layer) attaches on the posterior edge of the scapula, running downward to anchor on the point of elbow. Signs and Symptoms: When the muscle is tight and the horse is at rest, he will hold his leg bent (flexed) and will not lock the knee joint completely. It runs downwards to each side to attach to the medial (internal) aspect of the humerus. Its contraction assists the protraction, controls the adduction, and assists the lateral movement of the foreleg. Signs and Symptoms: When tight, the muscle affects the stride and resists the abduction (lateral) movement of the foreleg. Stress point 15 will be felt as a rigid knot of tissues at the point it attaches to the humerus, and it will feel very tender to the horse. Signs and Symptoms: When tight, the muscle affects the stride and restricts the abduction movement of the foreleg. If the stress point is very tender, the horse will flinch and perhaps stamp his feet on the same side or try to pull away from the pres sure. Stress point 16 will be felt as a rigid knot of tissues by the attachment point on the humerus. During concentric contraction, it draws the foreleg backwards as well as assists in the adduction (medial) movement of the leg. During eccentric contraction this muscle assists in the abduction (lateral) movement of the foreleg. Signs and Symptoms: When this muscle is tight, the horse reacts to the tightening of the girth. During movement, the ani mal shows shortened extension of the foreleg and becomes stilted. Stress point 17 will be felt as a rigid knot of tissues on the ori gin tendon over the sternum. It will be a very sensitive area with a tight line of muscle fibers running forward along its course. Body Parts and Their Stress Points 213 #18 Stress Point—The Radial Carpal Extensor Muscles of the Foreleg Myology: the extensor muscles (located in the superficial layer) attach on the lower end of the humerus, running downwards to attach on the anterior aspect of the pastern bones. Signs and Symptoms: When these muscles are tight they limit the extension of the hoof during protraction of the leg. Stress point 18 will be felt as a rigid knot of tissues by the attachment point on the humerus.

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Syndromes

  • A suppressed immune system (immunosuppression), such as that caused by HIV infection or AIDS
  • Alcohol or drug abuse
  • Gastrin blood level
  • Shortness of breath that gets worse with exercise or activity
  • When the diagnosis is not clear, the doctor may order a CT scan or ultrasound to make sure the appendix is the cause of the problem.
  • Need many blood transfusions
  • Tricyclic antidepressants
  • Kidney x-rays (may show kidney stones)
  • Apathy