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Dictionary of Neurological Signs
Out of stock Notify me when available Submit. Check for new and used marketplace copies. The first two editions of the Dictionary of Neurological Signs were very well-received by readers and reviewers alike. Like those editions, this Third Edition, updated and expanded, can be almost as well described in terms of what the book is not, along with details about what it is.
The Dictionary is not a handbook for treatment of neurological disorders. While many entries provide the latest treatment options, up-to-the-minute therapies are not discussed in bedside level detail. The Dictionary is an alphabetical listing of commonly presenting neurological signs designed to guide the physician toward the correct clinical diagnosis. A wooden stick or pin is used to scratch the abdominal wall, from the flank to the midline, parallel to the line of the dermatomal strips, in upper supraumbilical , middle umbilical , and lower infraumbilical areas.
The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage upper motor neurone lesions above T6. All abdominal reflexes are preserved with lesions below T Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis variant of motor neurone disease from multiple sclerosis.
However, no prospective study of abdominal reflexes in multiple sclerosis has been reported. The deep tendon and the abdominal reflexes. Isolated weakness of the lateral rectus muscle may also occur in myasthenia gravis. This may be a barely noticeable suspension of speech or attentiveness, without postictal confusion or awareness that an attack has occurred, as in idiopathic generalized epilepsy of absence type absence epilepsy; petit mal , a disorder exclusive to childhood and associated with 3 Hz spike and slow wave EEG abnormalities.
There may also be some clinical overlap with catatonia. Abulia may result from frontal lobe damage, most particularly that involving the frontal convexity, and has also been reported with focal lesions of the caudate nucleus, thalamus, and midbrain. Pathologically, abulia may be observed in: Infarcts in anterior cerebral artery territory and ruptured anterior communicating artery aneurysms, causing basal forebrain damage.
There is anecdotal evidence that the dopamine agonist bromocriptine may help. Clinical features and current management of abulia. The behavioral and motor consequences of focal lesions of the basal ganglia in man. Brain ; Fisher CM. In: Bogousslavsky J, Caplan L eds. Stroke syndromes. Cambridge: CUP, Cross References Akinetic mutism; Apathy; Bradyphrenia; Catatonia; Frontal lobe syndromes; Psychomotor retardation Acalculia Acalculia, or dyscalculia, is difficulty or inability in performing simple mental arithmetic.
This depends on two processes, number processing and calculation; a deficit confined to the latter process is termed anarithmetia. Acalculia may occur in association with alexia, agraphia, finger agnosia, right-left disorientation, and difficulty spelling words as part of the Gerstmann syndrome with lesions of the dominant parietal lobe.
Secondary acalculia is the more common variety.
Impairments may be remarkably focal, for example one operation e. Aphasia: a clinical perspective. Acalculia: historical development and current significance. Brain and Cognition ; 2: Butterworth B. The mathematical brain. Acalculia and disturbances of body schema. Clinical neuropsychology 4th edition. Acalculia: a disorder of numerical cognition. Neurological foundations of cognitive neuroscience. Selective acalculia with sparing of the subtraction process in a patient with a left parietotemporal hemorrhage.
The isolation of calculation skills. This reflex is typically lost in polyneuropathies, S1 radiculopathy, and, possibly, as a consequence of normal ageing. Cross References Age-related signs; Neuropathy; Reflexes Achromatopsia Achromatopsia, or dyschromatopsia, is an inability or impaired ability to perceive colors. This may be ophthalmological or neurological in origin, congenital or acquired; only in the latter case does the patient complain of impaired color vision.
A Dictionary of Neurological Signs 2nd Edition - PDF Free Download
Achromatopsia is most conveniently tested for clinically using pseudoisochromatic figures e. Sorting colors according to hue, for example with the Farnsworth-Munsell Hue test, is more quantitative, but more time consuming. Difficulty performing these tests does not always reflect achromatopsia see Pseudoachromatopsia. These inherited dyschromatopsias are binocular and symmetrical and do not change with time.
Acquired achromatopsia may result from damage to the optic nerve or the cerebral cortex. Cerebral achromatopsia results from cortical damage most usually infarction to the inferior occipitotemporal area. Area V4 of the visual cortex, which is devoted to color processing, is in the occipitotemporal fusiform and lingual gyri. Unilateral lesions may produce a homonymous hemiachromatopsia. Lesions in this region may also produce prosopagnosia, alexia, and visual field defects, either a peripheral scotoma which is always in the upper visual field, or a superior quadrantanopia, reflecting damage to the inferior limb of the calcarine sulcus in addition to the adjacent fusiform gyrus.
Transient achromatopsia in the context of vertebrobasilar ischemia has been reported. Postgraduate Medical Journal ; Zeki S. A century of cerebral achromatopsia. There does seem to be an age-related loss of distal sensory axons and of spinal cord ventral horn motor neurones accounting for sensory loss, loss of muscle bulk and strength, and reflex diminution.
References Franssen EH. Neurological signs of aging. Principles and practice of geriatric medicine 4th edition. Chichester: Wiley, in press Cross References Frontal release signs; Parkinsonism; Reflexes Ageusia Ageusia or hypogeusia is a loss or impairment of the sense of taste gustation. This may be tested by application to each half of the protruded tongue the four fundamental tastes sweet, sour, bitter, and salt. Isolated ageusia is most commonly encountered as a transient feature associated with coryzal illnesses of the upper respiratory tract, as with anosmia.
Indeed, many complaints of loss of taste are in fact due to anosmia, since olfactory sense is responsible for the discrimination of many flavors. Neurological disorders may also account for ageusia. Afferent taste fibers run in the facial VII and glossopharyngeal IX cranial nerves, from taste buds in the anterior two-thirds and posterior onethird of the tongue respectively. Central processes run in the solitary tract in the brainstem and terminate in its nucleus nucleus tractus solitarius , the rostral part of which is sometimes called the gustatory nucleus.
Fibers then run to the ventral posterior nucleus of the thalamus, hence to the cortical area for taste adjacent to the general sensory area for the tongue insular region. Lesions of the facial nerve proximal to the departure of the chorda tympani branch in the mastoid vertical segment of the nerve A Agnosia i. Lesions of the glossopharyngeal nerve causing impaired taste over the posterior one-third of the tongue usually occur in association with ipsilateral lesions of the other lower cranial nerves X, XI, XII; jugular foramen syndrome and hence may be associated with dysphonia, dysphagia, depressed gag reflex, vocal cord paresis, anesthesia of the soft palate, uvula, pharynx and larynx, and weakness of trapezius and sternocleidomastoid.
Anosmia and dysgeusia have also been reported following acute zinc loss. Disturbances of taste and smell. Neurology in clinical practice 3rd edition. Sudden-onset ageusia in the antiphospholipid syndrome. As a corollary of this last point, there should be no language disorder aphasia for the diagnosis of agnosia. However, others retain this category, not least because the supposition that perception is normal in associative visual agnosia is probably not true.
Moreover, the possibility that some agnosias are in fact higher order perceptual deficits remains: examples include some types of visual and tactile recognition of form or shape e. Theoretically, agnosias can occur in any sensory modality, but some authorities believe that the only unequivocal examples are in the visual and auditory domains e.
With the passage of time, agnosic defects merge into anterograde amnesia failure to learn new information. Anatomically, agnosias generally reflect dysfunction at the level of the association cortex, although they can on occasion result from thalamic pathology. Some may be of localizing value.