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24 results

Page 1 of 2

  • 2 - Neuroradiology
    • from SECTION I - NEUROLOGICAL EXAMINATION AND NEURODIAGNOSTIC TESTING
    • By Andrew L. Goldberg, Director Westside imaging Center Brook Brook Park, Ohio, Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 12-29
  • View abstract

    Summary

    Magnetic resonance imaging (MRI) with or without contrast is the study of choice when cerebellar, brainstem, or internal auditory meatus pathology is suspected. Similarly, the yield of computed tomography (CT) brain scans is minimal in patients with syncope or near syncope. Suspected spinal cord compression is best defined by MRI. Traumatic or atraumatic myelopathy should be investigated with emergent MRI. In case of nontraumatic myelopathy, the entire spine must be evaluated by MRI. Ready access to CT and its accurate interpretation is essential in evaluating the patient presenting with a new ischemic neurological deficit. Epidural hematomas are often associated with skull fractures, which should be evaluated with CT bone settings and the plain radiography. Most of epidural hematomas result from laceration of the meningeal arteries and/or dural venous sinuses. MRI is particularly sensitive in demonstrating subacute subdural hematomas because of its inherent soft tissue contrast characteristics and its multiplanar capability.
  • SECTION II - COMMON NEUROLOGICAL PRESENTATIONS
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    Altered mental status is due to neuronal dysfunction on a cellular level due primarily to inadequate oxygenation or glucose delivery to the cell. Abnormal vital signs are noted. Arrhythmias, especially atrial fibrillation and ventricular tachycardias, suggest an ischemic, toxic, or multifocal embolic etiology but also occur in dehydration or stress. Hypertension when extreme (diastolic greater than 120 mm Hg) can cause coma in hypertensive encephalopathy. A nonfocal neurological exam directs the work-up toward an etiology affecting the cortex diffusely, causing encephalopathy. Initial laboratory testing includes basic chemistries, glucose, creatinine, blood urea nitrogen, urinalysis and urine culture, and arterial blood gases. Administration of dextrose and thiamine is warranted in those patients in whom the etiology of the mental status change is unclear and the neurological examination is non-focal. The Glasgow Coma Scale has been shown to help prognosticate recovery in coma resulting both from trauma and out-of-hospital cardiac arrest.
  • 26 - Nontraumatic Spinal Cord Emergencies
    • from SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 263-272
  • View abstract

    Summary

    Nontraumatic spinal emergencies can be caused by a wide spectrum of conditions including infection, hemorrhage, and neoplasm. The most common findings in patients with spinal emergencies are pain, motor deficits, sensory deficits, abnormal reflexes, and urinary dysfunction. Acute back pain is the only symptom of catastrophic spinal emergencies such as spinal hemorrhage or infection. Sudden paralysis can result from trauma, cord infarction, or hemorrhage. Even though a thorough sensory examination in the emergency department is often difficult and unreliable, complexes of sensory and motor abnormalities are helpful. As a result of the anatomical distribution of upper and lower motor neurons, acute spinal cord lesions almost always present with hyperreflexia. The mechanism of urinary incontinence depends on the type of lesion. Spinal cord emergencies frequently go unrecognized initially or are misdiagnosed even with such obvious symptoms as the inability to walk or bladder function failure.
  • 24 - Idiopathic Intracranial Hypertension
    • from SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 252-259
  • View abstract

    Summary

    Idiopathic intracranial hypertension (IIH) is considered when evaluating a young patient with symptoms such as headache, transient visual obscuration or finding of palliedema. Lumbar puncture (LP) with opening pressure recording and cerebrospinal fluid (CSF) examination are required in patients with suspected IIH. Patients with IIH can have large variations in intracranial pressure (ICP), but rarely a single measurement of ICP is normal. Pathological conditions that resemble IIH clinically include cerebral mass lesions, hypertensive encephalopathy, hydrocephalus, and dural sinus thrombosis. Chronic forms of meningitis such as cryptococcal meningitis can resemble IIH initially because of headache and papilledema. Changes in visual acuity or visual-evoked potentials are signs of end-stage IIH-related optic nerve injury. Hospitalization is required when rapid visual loss or serious complications of IIH are suspected. Consultation with a neurologist, ophthalmologist, and neurosurgeon is indicated according to the severity of symptoms and the current treatment.
  • 35 - Hypotonic Infant
    • from SECTION V - PEDIATRIC NEUROLOGICAL EMERGENCIES
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 350-358
  • View abstract

    Summary

    A focused history and a careful physical examination of a hypotonic infant distinguish hypotonia from weakness, essential to diagnosis and treatment. The differential diagnosis of infantile hypotonia can be generated by first determining whether hypotonia is associated with weakness. Global central nervous system (CNS) disorders are suggested by the loss of developmental milestones or evidence of mental retardation. The disorders associated with significant weakness and secondary hypotonia are: spinal muscular atrophy or Werdnig-Hoffmann syndrome, congenital muscular dystrophies, congenital myotonic dystrophy and Guillain-Barré syndrome. Hypotonia with weakness requires the use of electrophysiology and biopsy studies, interpreted in the context of the infant's age. Hospitalization is commonly required to observe a hypotonic infant and to continue with diagnostic evaluation. A pediatric neurologist is consulted to determine the need for further diagnostic procedures or to initiate treatment of an underlying neurological disorder.
  • SECTION VII - NEUROTOXICOLOGY
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    Many poisonous substances produce their primary toxic effects by affecting neurotransmission. Recognition of several known toxidromes may narrow the diagnostic focus and aid in management. The various types of toxidromes include: cholinergic syndrome, aticholinergic syndrome, adrenergic syndrome, sedative hypnotic syndrome, opioid syndrome, and withdrawal syndromes. Although many drugs depress the level of consciousness and respiratory drive, the agents most frequently responsible for these effects include opioids or sedative/hypnotics. The toxicity from any of these agents can cause hypotension, hypothermia, pulmonary edema, and hyporeflexia. Electrical injuries can result in numerous immediate and delayed neurological complications. The most common cause of death by either alternating current or direct current (lightning strike) is cardiorespiratory arrest. The most common cause of death in persons with significant thermal injury is multiple organ failure and its complications. Alternating current typically induces ventricular fibrillation and lightning strike (direct current) commonly causes asystole.
  • SECTION IV - NEUROLOGICAL TRAUMA
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    Patients with mild traumatic brain injury (TBI) can have normal neurological and physical examinations. Mild traumatic brain injury is not always clinically apparent. The findings include: any period of loss of consciousness, amnesia of the event, and change in mental status such as feeling dizzy or disoriented. Focal motor findings in the unconscious patient with TBI can localize intracranial lesions or spinal cord injuries. Noncontrast computerized tomography (CT) provides useful anatomical and pathological information regarding the location, extent, and nature of the TBI within minutes. Although available evidence does not show that prevention of early posttraumatic seizures improves outcomes following TBI, anticonvulsants are an option in patients at high risk for seizures following head injury (Glasgow Coma Scale less than 9). TBI is the cause of death in approximately 40% of childhood injuries, and occurs more frequently in males and infants or adolescents.
  • 15 - Guillain-Barré Syndrome
    • from SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
    • By Sandeep Rana, Department of Neurology Allegheny General Hospital Pittsburgh, Pennsylvania, Sid M. Shah, Assistant Clinical Professor Michigan State University
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 175-179
  • View abstract

    Summary

    Guillain-Barré syndrome (GBS) is a form of acute inflammatory (demyelinating) polyneuropathy. It causes rapidly ascending numbness and weakness. In the early phase, a high index of suspicion for GBS is essential in the presence of ascending numbness and weakness because ancillary tests may not help. A normal cerebrospinal fluid (CSF) protein level in the early phase or a finding of numerous lymphocytes does not exclude the diagnosis of GBS. By end of first week of illness, CSF analysis usually reveals normal CSF pressure and elevated protein without leukocytosis termed albuminocytological dissociation. Despite advances in the treatment of GBS, good supportive care is still the most important determinant of favorable outcome. Cardiac monitoring is routine for patients with severe findings. Respiratory status is assessed with periodic vital capacities. Elective endotracheal intubation for ventilatory support is considered when the vital capacity is below 15 ml/kg.
  • SECTION I - NEUROLOGICAL EXAMINATION AND NEURODIAGNOSTIC TESTING
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    A detailed neurological history allows one to focus on important components of the neurological examination and for saving time and resources. The important elements of a focused neurological examination include onset of symptoms, temporal relationships of symptoms, progression of symptoms, associated symptoms, exacerbating and alleviating factors, symptoms that indicate involvement of a particular region of central nervous system (CNS), history of similar event and history of medication use. This chapter describes the examination of mental status, cranial nerve function, motor function, deep tendon reflexes, cutaneous reflexes, and miscellaneous signs, sensory modalities, and pathological reflexes. The Glasgow Coma Scale is often used as a method of briefly quantitating neurological dysfunction. A simple method to remember the anatomic basis of neurological examination is to focus on five levels of the CNS, which are the brain, the brainstem, the spinal cord, the peripheral nerves, and the muscles.
  • 28 - Traumatic Brain Injury
    • from SECTION IV - NEUROLOGICAL TRAUMA
    • By Christopher Carpenter, Departments of Emergency and Internal Medicine University St. Louis, Missouri, Kevin Gingrich, Department of Anesthesiology Thomas Jefferson University Philadelphia, Pennsylvania, James E. Wilberger, Department of Neurology Allegheny General Hospital Pittsburgh, Pennsylvania, Lee Warren, Department of Neurology Wildford Hall Air Force Medical Center San Antonio, Texas, Sid M. Shah, Assistant Clinical Professor Michigan State University
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 279-285
  • View extract

    Summary

    Patients with mild traumatic brain injury (TBI) can have normal neurological and physical examinations. Mild traumatic brain injury is not always clinically apparent. The findings include: any period of loss of consciousness, amnesia of the event, and change in mental status such as feeling dizzy or disoriented. Focal motor findings in the unconscious patient with TBI can localize intracranial lesions or spinal cord injuries. Noncontrast computerized tomography (CT) provides useful anatomical and pathological information regarding the location, extent, and nature of the TBI within minutes. Although available evidence does not show that prevention of early posttraumatic seizures improves outcomes following TBI, anticonvulsants are an option in patients at high risk for seizures following head injury (Glasgow Coma Scale less than 9). TBI is the cause of death in approximately 40% of childhood injuries, and occurs more frequently in males and infants or adolescents.
  • SECTION VI - PREGNANCY-RELATED NEUROLOGICAL EMERGENCIES
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    When convulsions and altered sensorium occur in the pregnant patient past 20 weeks gestation or in the first 2 weeks postpartum, eclampsia is the prime suspect. Phenytoin can be used to control seizures that are resistant to magnesium. Phenytoin is also a good choice if a woman is identified as high risk for eclamptic seizures and needs treatment for a prolonged period of time. Adequate control of hypertension is essential for prevention of central nervous system (CNS) complications in these patients. All patients with eclampsia and many with preeclampsia need hospitalization. Seizures are one of the most frequent neurological disorders encountered in pregnancy and carry an increased risk to the fetus from trauma, hypoxia, and metabolic acidosis. Quite common during pregnancy, headache is generally benign, but it can occasionally herald serious pathology. Chorea gravidarum (CG) is chorea occurring during pregnancy. Myasthenia gravis (MG) worsens in 40% of women with pregnancy.
  • SECTION VIII - BRAIN DEATH
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    The brain death criteria include assessment of the following: normothermia; cause of brain death; unresponsiveness; absence of brainstem reflexes; and apnea. The presence of withdrawal reflexes, typically seen in the lower extremities, do not preclude the diagnosis of brain death given that withdrawal reflexes can be spinally mediated. The absence of brainstem reflexes includes pupillary responses, eye movements, and lower brainstem reflexes such as response to tracheal stimulation. Apnea testing is performed to demonstrate lack of respiratory effort, even in the presence of elevated pCO2 levels. When no respiratory effort is made during the apnea test and the other criteria have been met, the patient may be pronounced dead. The diagnosis of brain death is not without controversy. For instance, thermoregulation is regarded as a brainstem function; therefore, some argue that those patients who maintain their body temperature cannot be declared brain dead.
  • SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan, Kevin M. Kelly, Associate Professor of Neurology Drexel University College of Medicine
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp -
  • View abstract

    Summary

    Central nervous system (CNS) infections range from rapidly fatal bacterial meningitis to slowly progressive infectious processes from mycobacterial, fungal, or viral agents. The diagnosis of acute bacterial meningitis is made by the examination of cerebrospinal fluid (CSF). Brain abscess is a suppurative infection involving brain parenchyma. Although the CNS infections most commonly associated with HIV infection are toxoplasmosis and cytomegalovirus (CMV), such patients are susceptible to many other infections including aseptic meningitis, neurosyphilis, and M. tuberculosis. The term aseptic meningitis has been used to describe conditions of acute meningeal irritation that prove to be benign and self-limiting. The incidence of tuberculosis (TB) is on the rise, due to an increase in numbers of HIV-infected persons, numbers of homeless individuals, and immigrants from developing countries. Cryptococcus neoformans, a common fungal pathogen, commonly affects HIV infected patients. Viral encephalitis is an infectious and inflammatory process involving the brain.
  • 13 - Movement Disorders
    • from SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
    • By Sid M. Shah, Assistant Clinical Professor Michigan State University, Roger Albin, Department of Neurology University of Michigan Ann Arbor, Michigan, Susan Baser, Department of Neurology Allegheny General Hospital Pittsburgh, Pennsylvania
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 146-160
  • View abstract

    Summary

    Movement disorders (MD) encountered in the emergency department (ED) range from the familiar Parkinsonism and drug-induced dystonias to rare disabling hemiballism secondary to a stroke. Movement disorders can be classified into four broad categories based on phenomenological features, clinical pharmacology, and neuropathology. It includes hypokinetic disorders identical to Parkinsonism's syndrome, hyperkinetic/choreic movement disorders, tremors, and myoclonus. The cause-and-effect relationship between the drug and the movement disorder is poorly understood, but preexisting central nervous system (CNS) pathology likely predisposes to the development of movement disorders. Commonly prescribed medications that result in movement disorders include antiepileptics, neuroleptics, stimulants, oral contraceptives, antihistaminics and anticholinergics, and antidepressants. The use of monoamine oxidase (MAO) inhibitors is associated with tremors and less often with myoclonic jerks. Tricyclic antidepressants such as amitriptyline, imipramine, and nortriptyline cause choreiform movements infrequently, particularly orofacial dyskinesia.
  • 23 - Increased Intracranial Pressure and Herniation Syndromes
    • from SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
    • By Amy Blasen, Sparrow Healthcare System Sparrow Hospital/MSU Emergency Medicine Residency Program Lansing, Michigan, Sid M. Shah, Assistant Clinical Professor Michigan State University
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 242-251
  • View abstract

    Summary

    Primary survey of a patient suspected of having an increased intracranial pressure (ICP) consists of a brief neurological examination and establishment of a Glasgow Coma Scale (GCS) score. Brain herniation, an end-stage manifestation of increased ICP, refers to displacement of brain tissue from one intracranial compartment to another through an opening in the dural sheath. A herniation syndrome is a neurosurgical emergency; if immediate intervention is not taken, death can ensue rapidly. Initial therapy is aimed at lowering ICP while determining and treating the underlying cause. Common conditions resulting in increased ICP include traumatic brain injury (TBI), cerebrovascular events, hydrocephalus, brain tumor, central nervous system infections, metabolic and hypoxic encephalopathies, and status epilepticus. Mannitol, an osmotic diuretic, is currently the diuretic of choice for treating increased ICP. Barbiturate therapy is effective in lowering ICP in a select subset of patients such as those with persistently high ICP despite aggressive management.
  • 1 - Neurological Examination
    • from SECTION I - NEUROLOGICAL EXAMINATION AND NEURODIAGNOSTIC TESTING
    • By Thomas F. Scott, Department of Neurology Allegheny General Hospital Pittusburgh, Pennsylvania, Sid M. Shah, Assistant Clinical Professor Michigan State University; Faculty member of Sparrow/MSU Emergency Medicine Residency Program Lansing, Michigan
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book: Principles and Practice of Emergency Neurology
  • Published online: 06 August 2009
  • Print publication: 18 February 2003, pp 1-11
  • View extract

    Summary

    A detailed neurological history allows one to focus on important components of the neurological examination and for saving time and resources. The important elements of a focused neurological examination include onset of symptoms, temporal relationships of symptoms, progression of symptoms, associated symptoms, exacerbating and alleviating factors, symptoms that indicate involvement of a particular region of central nervous system (CNS), history of similar event and history of medication use. This chapter describes the examination of mental status, cranial nerve function, motor function, deep tendon reflexes, cutaneous reflexes, and miscellaneous signs, sensory modalities, and pathological reflexes. The Glasgow Coma Scale is often used as a method of briefly quantitating neurological dysfunction. A simple method to remember the anatomic basis of neurological examination is to focus on five levels of the CNS, which are the brain, the brainstem, the spinal cord, the peripheral nerves, and the muscles.

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