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Diovascular Reflexes, Comprising Forced Expiration Against Resistance (“Straining”), Followed by Release of the Resistance and Completion of Expiration

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Diovascular Reflexes, Comprising Forced Expiration Against Resistance (“Straining”), Followed by Release of the Resistance and Completion of Expiration V.qxd 9/28/05 10:49 PM Page 316 V Valsalva Maneuver The Valsalva maneuver is a simple test of autonomically-mediated car- diovascular reflexes, comprising forced expiration against resistance (“straining”), followed by release of the resistance and completion of expiration. The first phase produces impaired cardiac filling due to impaired venous return as a consequence of elevated intrathoracic pressure, with a fall in cardiac output and blood pressure, inducing peripheral vasoconstriction (sympathetic pathways) to maintain blood pressure. The second phase causes a transient overshoot in blood pres- sure as the restored cardiac output is ejected into a constricted circu- lation, followed by reflex slowing of heart rate. In autonomic (sympathetic) dysfunction, reflex vasoconstriction, blood pressure overshoot and bradycardia do not occur. The latter may be conveniently assessed by measuring R-R intervals in a prolonged ECG recording, an R-R interval ratio between the straining and release phases of less than 1.1 suggesting impaired baroreceptor response. Cross References Orthostatic hypotension Vegetative States The vegetative state is a clinical syndrome in which cognitive function is lost, due to neocortical damage (hence no awareness, response, speech), while vegetative (autonomic, respiratory) function is pre- served due to intact brainstem centres. Primitive postural and reflex limb movements may also be observed. The syndrome, also known as neocortical death, coma vigil, and the apallic syndrome, may be seen after extensive ischemic-hypoxic brain injury, for example following resuscitation after cardiac arrest, and needs to be distinguished from coma, akinetic mutism, and the locked-in syndrome. Persistent vegeta- tive state (PVS) is defined by persistence of this state for > 12 months (UK) or > 6 months (USA) after brain trauma, or > 6 months (UK) or > 3 months (USA) following brain anoxia. The prognosis of PVS is poor, but occasional reports of very late recovery have appeared. References Jennett B. The vegetative state. Medical facts, ethical and legal dilem- mas. Cambridge: CUP, 2002 Wade DT, Johnston C. The permanent vegetative state: practical guidelines on diagnosis and management. British Medical Journal 1999; 319: 841-844 Zeman A. The persistent vegetative state: conscious of nothing? Practical Neurology 2002; 2: 214-217 Cross References Akinetic mutism; Coma; Locked-in syndrome - 316 - V.qxd 9/28/05 10:49 PM Page 317 Vertigo V Venous Pulsation - see RETINAL VENOUS PULSATION Vernet’s Syndrome - see JUGULAR FORAMEN SYNDROME Vertigo Vertigo is an illusion of movement, a sense of rotation or of tilt, caus- ing a feeling of imbalance or dysequilibrium. It is a subtype of “dizzi- ness’, to be distinguished from the light-headedness of general medical conditions (vasovagal attacks, presyncope, cardiac dysrhythmias). Vertigo is often triggered by head movement and there may be associ- ated autonomic features (sweating, pallor, nausea, vomiting). Vertigo may be horizontal, vertical or rotatory. Pathophysiologically, vertigo reflects an asymmetry of signaling anywhere in the central or peripheral vestibular pathways. Clinically it may be possible to draw a distinction between central and peripheral lesions: in the latter there may be concurrent hearing loss and tinnitus (reflecting vestibulocochlear (VIII) nerve involvement). Facial weak- ness (VII) and ipsilateral ataxia suggest a cerebellopontine angle lesion; diplopia, bulbar dysfunction and long tract signs are suggestive of a central pathology. Peripheral vertigo tends to compensate rapidly and completely with disappearance of nystagmus after a few days, whereas central lesions compensate slowly and nystagmus persists. The clinical pattern of vertigo may gives clues as to underlying diagnosis: Vertigo Peripheral Central Acute Labyrinthitis Prolonged, Otomastoiditis Brainstem/ spontaneous Vestibular neur(on)itis cerebellum Labyrinthine concussion hemorrhage/ Isolated labyrinthine infarct infarct/ Vestibular nerve section demyelination Drug-induced Recurrent, Ménière’s disease Vertebrobasilar episodic (endolymphatic hydrops) ischemia (with Autoimmune inner ear associated disease (isolated, systemic) features) Perilymph fistula Migraine (rare) Epilepsy (rare) Positional Benign paroxysmal 4th ventricle positional vertigo (BPPV) lesions: multiple sclerosis Chiari malformation (contd.) - 317 - V.qxd 9/28/05 10:49 PM Page 318 V Vestibulo-Ocular Reflexes (contd.) Vertigo Peripheral Central Brainstem/ cerebellar tumors Spinocerebellar atrophy Chronic Vestibular Neurological decompensation/failure disorder Psychogenic All patients with vertigo should have a Hallpike maneuver performed during the examination. Specific treatments are available for certain of these conditions. A brief course of a vestibular sedative (cinnarizine, Serc) is appropri- ate in the acute phase, but exercises to “rehabilitate” the semicircular canals should be begun as soon as possible in peripheral causes. In BPPV, most patients respond to the Epley maneuver to reposition the otoconia which are thought to cause the condition (canalolithiasis). Brandt-Daroff exercises are an alternative. Cawthorne-Cooksey exer- cises are helpful in vestibular decompensation or failure. References Baloh RW. Vertigo. Lancet 1998; 352: 1841-1846 Brandt T. Vertigo: its multisensory syndromes (2nd edition). London: Springer, 1999 Hain TC, Uddin MK. Approach to the patient with dizziness and ver- tigo. In: Biller J (ed.). Practical neurology (2nd edition). Philadelphia: Lippincott Williams & Wilkins, 2002: 189-205 Luxon LM. Vertigo: new approaches to diagnosis and management. British Journal of Hospital Medicine 1996; 56: 519-520, 537-541 Cross References Ataxia; Caloric testing; Facial paresis; Hallpike maneuver, Hallpike test; Hennebert’s sign; Illusion; Nystagmus; Vestibulo-ocular reflexes Vestibulo-Ocular Reflexes The vestibulo-ocular reflexes (VOR) are a physiological mechanism which generates eye rotations that compensate for head movements, especially during locomotion, so stabilizing the retinal image on the fovea. VORs depend upon the integrity of the connections between the semicircular canals of the vestibular system (afferent limb of reflex arc) and oculomotor nuclei in the brainstem (efferent limb). Loss of vestibular function, as in acute bilateral vestibular failure, causes gaze instability due to loss of VORs, causing the symptom of oscillopsia (q.v.) when the head moves. As well as vestibular input, compensatory eye rotations may also be generated in response to visual information (pursuit-optokinetic eye movements) and neck proprioceptive information; anticipatory eye movements may also help stabilize the retinal image. - 318 - V.qxd 9/28/05 10:49 PM Page 319 Vibration V VORs are also useful in assessing whether ophthalmoplegia results from a supranuclear or infranuclear disorder, since in the former the restriction of eye movement may be overcome, at least in the early stages, by the intact VOR (e.g., the supranuclear gaze palsy in the vertical plane in progressive supranuclear palsy). VORs are difficult to assess in conscious patients because of con- current pursuit-optokinetic eye movements, and because rotation of the head through large angles in conscious patients leads to interruption of VORs by vestibular nystagmus in the opposite direction (optokinetic nystagmus). The head impulse test (q.v.) may be used to test VORs in conscious patients, for example those with vertigo in whom vestibular failure is suspected. VOR may also be assessed using a slow (0.5-1.0 Hz) doll’s head maneuver while directly observing the eyes (“catch up” sac- cades may be seen in the absence of VOR), measuring visual acuity (dynamic visual acuity, or illegible E test; dropping two to three lines on visual acuity with head movement vs. normal if VOR impaired), and ophthalmoscopy (optic disc moves with head if VOR abnormal). In unconscious patients, slow phase of the VORs may be tested by rotating the head and looking for contraversive conjugate eye move- ments (oculocephalic responses, doll’s head eye movements) or by caloric testing. VORs are lost in brainstem death. Another important element of VOR assessment is suppression or cancellation of VOR by the pursuit system during combined head and eye tracking. VOR suppression may be tested by asking the patient to fixate on their thumbs with arms held outstretched while rotating at the trunk or sitting in a swivel chair. VOR suppression can also be assessed during caloric testing: when the nystagmus ceases with fixation, removal of the fixation point (e.g., with Frenzel’s glasses) will lead to recurrence of nystagmus in normals but not in those with reduced or absent VOR suppression. VOR suppression is impaired (presence of nystagmus even with slow head movements) in cerebellar and brainstem disease. References Bronstein AM. Vestibular reflexes and positional manoeuvres. Journal of Neurology, Neurosurgery and Psychiatry 2003; 74: 289-293 Leigh RJ, Brandt T. A reevaluation of the vestibulo-ocular reflex: new ideas of its purpose, properties, neural substrate, and disorders. Neurology 1993; 43: 1288-1295 Cross References Caloric testing; Coma; Doll’s eye maneuver, Doll’s head maneuver; Hallpike maneuver, Hallpike test; Head impulse test; Ocular tilt reac- tion; Oculocephalic response; Oscillopsia; Supranuclear gaze palsy; Vertigo Vibration Vibratory sensibility (pallesthesia) represents a temporal modulation of tactile sense. On this ground, some would argue that the elevation
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