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This chapter describes methods of clinical history taking and examination of the PLDD candidate with lumbar radicular symptoms. It stresses features of the classical neurological examination of the back and lower extremities in a concise, systematic fashion.
For the past decade, our group of neurologists, biomedical engineers and statisticians has developed objective tests to quantify apropos neurological functions (cognition, strength, steadiness, reactions, speed, coordination, sensations, fatigue, gait, station and selected skills of daily living). Instrumented tests have been extensively evaluated and used in several randomized double-blind trials in multiple sclerosis and Parkinson's disease. Our long-term goal is to bring to clinical neurology a type of quantification of the nervous system which does not exist. In this report, a brief overview of test development, personnel training, test administration and selected situations for using the clinical quantitative neurological examination (CQNE) are discussed. In addition, 57 tests are illustrated and described.
Of the proliferating approaches to neuropsychiatric assessment, a relatively neglected technique is the venerable, accessible, noninvasive, and inexpensive neurologic examination. This article organizes and synthesizes the literature on neurological findings in adult psychiatric patients. Problems in conducting and interpreting research in this area are examined, clinically pertinent empirical findings are surveyed, and directions for future investigation are outlined. Most of the "soft signs" can be reliably evaluated, and many have been validated against other techniques. Several psychiatric diagnoses are associated with impaired neurologic performance. Prognosis and treatment selection may also be informed by neurologic findings. The neurologic exam should be regarded as a collection of neurobiologic probes rather than as a single irreducible variable. Future work must better establish interrater and test-retest reliability of individual elements of the neurologic exam in psychiatric populations and focus on developing the clinical utility of individual and combined elements of the neurologic exam.
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RATIONALE AND OBJECTIVES: Magnetic resonance imaging has become a standard screening tool in the evaluation of patients with complex partial seizures. This study prospectively addresses the efficacy, if any, of routinely adding gadolinium-enhanced images to routine T2-weighted images in patients with a normal neurologic examination. METHODS: One hundred consecutive patients with electroencephalogram and clinical evidence of complex partial seizures and no other neurologic abnormalities were examined prospectively with axial and coronal T2-weighted spin-echo images, followed by axial and coronal gadolinium-enhanced T1-weighted scans. RESULTS: The scans in 73 patients were interpreted as normal, 14 had nonspecific white matter lesions, 5 had asymmetry of the temporal horns, and 2 had asymmetric signal intensity in the temporal lobes, and the scans in 6 showed abnormal gadolinium enhancement. Of the lesions in the six patients whose scans showed abnormal enhancement, four were seen well on the T2-weighted images. Of the remaining two, one was a small cerebellar venous angioma, and the other, a probable tiny convexity meningioma. One temporal lobe glioma seen on the T2 scans did not enhance with gadolinium. CONCLUSIONS: Routine administration of gadolinium does not appear to be of benefit in imaging patients with complex partial seizures who are otherwise neurologically normal.
OBJECTIVE: To determine the sensitivity and specificity of clinical tests for detecting focal lesions in a prospective blinded study. METHODS: 46 patients with a focal cerebral hemisphere lesion without obvious focal signs and 19 controls with normal imaging were examined using a battery of clinical tests. Examiners were blinded to the diagnosis. The sensitivity, specificity, and positive and negative predictive values of each test were measured. RESULTS: The upper limb tests with the greatest sensitivities for detecting a focal lesion were finger rolling (sensitivity 0.33 (95% confidence interval, 0.21 to 0.47)), assessment of power (0.30 (0.19 to 0.45)), rapid alternating movements (0.30 (0.19 to 0.45)), forearm rolling (0.24 (0.14 to 0.38)), and pronator drift (0.22 (0.12 to 0.36)). All these tests had a specificity of 1.00 (0.83 to 1.00). This combination of tests detected an abnormality in 50% of the patients with a focal lesion. In the lower limbs, assessment of power was the most sensitive test (sensitivity 0.20 (0.11 to 0.33)). Visual field defects were detected in 10 patients with a focal lesion (sensitivity 0.22 (0.12 to 0.36)) and facial weakness in eight (sensitivity 0.17 (0.09 to 0.31)). Overall, the examination detected signs of focal brain disease in 61% of the patients with a focal cerebral lesion. CONCLUSIONS: The neurological examination has a low sensitivity for detecting early cerebral hemisphere lesions in patients without obvious focal signs. The finger and forearm rolling tests, rapid alternating movements of the hands, and pronator drift are simple tests that increase the detection of a focal lesion without greatly increasing the length of the examination.
Sixty-seven patients with different stages of human immunodeficiency virus (HIV) infection (47 CDC group IV, 20 CDC groups II or III) were followed prospectively for a median of 18 months with neurological examination, magnetic resonance imaging (MRI), and computerized tomography (CT) to evaluate the incidence of the AIDS dementia complex (CDC definition) and other neurological complications. Ten patients developed CNS opportunistic infection or malignancy. Among the remaining 57 patients, 12 of 37 (32%) belonging to CDC group IV, and 1 of 20 (5%) belonging to CDC groups II/III developed the AIDS dementia complex (p = 0.03). MRI white matter lesions occurred in 32% of CDC group IV patients and 5% of CDC groups II/III patients (p = 0.03). The corresponding figures for brain atrophy at CT were 71% and 30% (p less than 0.01) and for neurologic signs 49% and 20% (p = 0.06). The development of the AIDS dementia complex was significantly associated with the occurrence of MRI white matter lesions and a CD4 cell count of less than 200 x 10(6)/l, whereas it was not statistical significantly associated with brain atrophy at baseline. It is concluded that the AIDS dementia complex is a common feature of late stage HIV infection. Brain atrophy occurs in a large percentage of HIV infected patients, but the clinical significance of this atrophy is not clear.
The authors report preliminary findings from an ongoing prospective study of neuroleptic-naive patients with first-break schizophrenia. They evaluated 17 of these patients and 15 normal subjects with a structured neurological examination before the patients received any medical treatment. The patients with schizophrenia showed significantly greater neurological impairment than did the normal comparison subjects.
The aim of this study was to develop and validate a simple, quantifiable, neurologic examination for infants between 2 and 24 months of age. The assessment consists of 37 items, divided into 3 sections. The first section includes 26 items assessing cranial nerve function, posture, movements, tone, and reflexes; the second section of 8 items documents the development of motor function, and the third section of 3 items evaluates the state of behavior. We applied this assessment to a cohort of ninety-two 12-month-old infants and forty-three 18-month-old infants, with no known perinatal risk factors. The proforma presented has been designed according to the frequency distribution of the neurologic findings in this cohort. Each item is scored individually, and a global score is the sum of all individual scores. The quantitative score enhances the value of this examination, both in clinical practice and in research settings.
The effect of induction of labour on the foetus and the newborn was investigated in a prospective randomized study. 41 neonates were studied after induction at full term by amniotomy and intravenous oxytocin infusion. The infusion rate was regulated by the intraamniotic pressure using the Cardiff infusion pump system. 39 neonates served as controls where the labour started spontaneously followed by amniotomy. In both groups foetal heart rate monitoring intraamniotic pressure recordings were performed. There were no differences in Apgar score and pH in cord blood between the groups. The newborns were evaluated the first and the fifth day of life with the Brazelton Neonatal Behavioral Assessment Scale and with a modified Prechtl neurological examination. There were no differences in behaviour and neurological state between the two groups. However, within the groups there were significant differences between the first and the fifth day concerning both neonatal behaviour and neurological state.
Thirty-six patients admitted with severe head injury and various degrees of systemic hypotension were studied to determine the effect of hypotension on the validity of the neurological examination in reflecting mechanical brain compression. All patients had clinical signs of transtentorial herniation or upper brainstem compression and underwent immediate bilateral placement of exploratory burr holes for the diagnosis and removal of intracranial hematomas. All patients were initially hypotensive: 10 were in cardiac arrest, 7 had a systolic blood pressure (SBP) less than 60 torr, and 19 had SBP of 60-90 torr. The median score on the Glascow coma scale was 3 (range 3-8). Although 4 of the 10 cardiac arrest patients had anisocoria, only one (10%) had an intracranial hematoma. Among the seven patients with severe hypotension, only two had anisocoria and neither had and intracranial hematoma; one patient in this group (14%) had a hematoma that was diagnosed at autopsy. In contrast, intracranial hematomas were discovered by burr-hole placement and evacuated in 13 (68%) of 19 patients with initially moderate hypotension, including seven (78%) of nine patients with anisocoria. Anisocoria was associated with mechanical brain compression from an intracranial hematoma significantly more often in patients with an initial SBP of 60-90 torr than in those with initial cardiac arrest or SBP less than 60 torr (chi-square p less than 0.05). Intracranial hematomas were significantly more frequent among patients with SBP of 60-90 torr than among those with a lower SBP or initial cardiac arrest (P less than 0.01). Thirty-three of 36 patients died; each of the three survivors had an initial SBP of 60-90 torr, and hematomas were removed in two. In head-injured patients with SBP greater than 60 torr, clinical signs of tentorial herniation or upper brainstem dysfunction remain valid indicators of possible mechanical compression; the high percentage of patients with acute intracranial hematomas in this group warrants immediate diagnostic burr-hole exploration. In patients with severe initial hypotension (SBP less than 60 torr) or cardiac arrest, clinical findings of brainstem dysfunction cannot be relied upon to indicate mechanical compression, and computed tomography scanning should be done immediately after resuscitation to determine the need for surgical exploration.
The frequency of abnormal findings at neurological examination was analyzed in an unselected sample of elderly people aged 67-87 years. Absent deep tendon reflexes and impairment of proprioceptive sensation rarely occurred in the elderly. Limitation of upward gaze and convergence appear a common finding, especially in the very old. Overall, the presence of cortical disinhibition signs (primitive reflexes and paratonia) did not discriminate well between subjects without CNS disease and demented patients. Only the presence of a prominent and persistent response to the stimulus and the number of cortical disinhibition signs found in the same subject appear useful criteria to distinguish between normality and dementia.
OBJECTIVE: Carbon disulphide (CS2) is highly neurotoxic. There is ample evidence of damage to the peripheral and central nervous system. The air concentration at which such adverse effects can first be observed is presently a subject of controversy. METHODS: In a cross-sectional study of CS2-exposed workers from the viscose industry and healthy controls, data on neurological complaints, basic laboratory diagnosis, clinical neurological examination and neuropsychological testing were evaluated. Data were from 222 workers in the viscose industry exposed to CS2 and 191 employees from the same factory with similar physical and psychological stress factors but without occupational contact with neurotoxic substances. Multiple linear or multiple logistic regression analysis was used to check for statistical differences. RESULTS: The median of the CS2-measurements using personal air sampling was below the current maximum concentration permissible (MAK value) in Germany (10 ppm) in all departments. The threshold limit value was, however, exceeded in almost 10% of the persons investigated. Exposure fluctuated between < 0.2 and 65.7 ppm (median of all departments was 4.02 ppm). As a parameter of internal exposure, CS2-metabolite 2-thio-1,3-thiazolidine-4-carboxylic acid (TTCA) concentrations in the urine of the exposed persons were between < 0.16 and 10.9 mg/g creatinine (median 1.43 mg/g). CONCLUSIONS: Neither an increase in subjective complaints nor an increase in pathological findings in clinical-neurological and neuropsychological examination could be found in persons exposed to CS2 at the exposure levels described.
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With practice, an orderly routine, and a basic understanding of neuroanatomy, the clinician should be able to tentatively localize lesions in the nervous system. Once the lesion is localized, ancillary studies are usually necessary to identify the disease process. In difficult cases when referral is impractical, an accurate description of the findings from the neurologic examination will greatly improve the value of consultation.
We have examined the incidence and size of infarction after occlusion of different portions of the rat middle cerebral artery (MCA) in order to define the reliability and predictability of this model of brain ischemia. We developed a neurologic examination and have correlated changes in neurologic status with the size and location of areas of infarction. The MCA was surgically occluded at different sites in six groups of normal rats. After 24 hr, rats were evaluated for the extent of neurologic deficits and graded as having severe, moderate, or no deficit using a new examination developed for this model. After rats were sacrificed the incidence of infarction was determined at histologic examination. In a subset of rats, the size of the area of infarction was measured as a percent of the area of a standard coronal section. Focal (1-2 mm) occlusion of the MCA at its origin, at the olfactory tract, or lateral to the inferior cerebral vein produced infarction in 13%, 67%, and 0% of rats, respectively (N = 38) and produced variable neurologic deficits. However, more extensive (3 or 6 mm) occlusion of the MCA beginning proximal to the olfactory tract--thus isolating lenticulostriate end-arteries from the proximal and distal supply--produced infarctions of uniform size, location, and with severe neurologic deficit (Grade 2) in 100% of rats (N = 17). Neurologic deficit correlated significantly with the size of the infarcted area (Grade 2, N = 17, 28 +/- 5% infarction; Grade 1, N = 5, 19 +/- 5%; Grade 0, N = 3, 10 +/- 2%; p less than 0.05). We have characterized precise anatomical sites of the MCA that when surgically occluded reliably produce uniform cerebral infarction in rats, and have developed a neurologic grading system that can be used to evaluate the effects of cerebral ischemia rapidly and accurately. The model will be useful for experimental assessment of new therapies for irreversible cerebral ischemia.
Vertigo is caused by disturbance of the input or central processing of sensory signals from the vestibular apparatus that provide information regarding the position of the body in space. It is caused either by asymmetric disruption of sensory input from the vestibular organs or asymmetric integration of vestibular input into the central nervous system. Vertigo is readily differentiated from other causes of dizziness by a sensation of motion. A crucial aspect of the management of the emergency department patient with vertigo is the differentiation of vertigo associated with acute stroke syndromes from vertigo due to peripheral causes. Routine computerized axial tomography imaging is insensitive for posterior circulation strokes, so for emergency physicians, the history and neurological examination remain the most useful diagnostic tools. This article emphasizes the history and physical examination in the localization of the lesion in patients with vertigo and offers a rational basis for decisions regarding the need for special neurological imaging and consultation. It also emphasizes subtle findings that may prevent the erroneous diagnosis of peripheral vertigo in the presence of an acute stroke syndrome.