05-21-2007, 08:34 PM
review of systems should concentrate on the evidence of bladder, kidney, lung, or skin infection and irritative or obstructive bladder symptoms.
Classic MS symptoms
Sensory loss (ie, paresthesias) usually is an early complaint.
Motor (eg, muscle cramping secondary to spasticity) and autonomic (eg, bladder, bowel, sexual dysfunction) spinal cord symptoms may be present.
Cerebellar symptoms (eg, Charcot triad of dysarthria, ataxia, tremor) may occur.
Constitutional symptoms, especially fatigue (which occurs in 70% of cases) and dizziness, may be present.
Subjective difficulties with attention span, concentration, memory, and judgment may be noted any time during the disease course.
About 50% of patients with MS have impairment, usually mild, in information processing on neuropsychological testing.
Depression is common, but euphoria is less common.
Over the course of the disease, 5-10% of patients develop an overt psychiatric disorder (eg, manic depression, paranoia, major depression) or dementia.
Eye symptoms, including diplopia on lateral gaze, occur in 33% of patients.
Trigeminal neuralgia may occur.
Optic neuritis (ON) (ie, inflammation or demyelination of optic nerve) is the initial presentation of 15% of patients with MS. Fifty percent of all patients who present with ON have MS. Isolated episodes of ON, even if they are recurrent, do not represent MS.
Acute onset (ie, occurring over minutes or hours, rarely days) of single eye visual blurring, decreased acuity (ie, usually scotoma), decreased color perception, and/or discomfort of the moving eye(s) are symptoms that are indicative of ON.
The 3 phenomena associated with ON or compressive/ischemic neuritis are as follows:
Phosphenes, or flashes of light, usually are precipitated by eye movements.
Uhthoff phenomenon or deterioration of vision is induced by exercise, a hot meal, or a hot bath.
The Pulfrich effect occurs when latencies between the eyes are unequal, resulting in a sense of disorientation in moving traffic.
Acute transverse myelitis
Partial acute transverse myelitis, rather than total, usually is a manifestation of MS. Strongly consider mechanical compression in the differential diagnosis.
Acute partial loss of motor, sensory, autonomic, reflex, and sphincter function below the level of the lesion indicates acute transverse myelitis.
Devic syndrome is acute transverse myelitis accompanied by bilateral ON.
Acute disseminated encephalitis is pathophysiologically and radiographically identical to MS. It is characterized by acute onset of motor, sensory, cerebellar, and cranial nerve dysfunction with encephalopathy, progressing to coma and eventual death in 30% of such cases.
MS as a sole symptom is unusual, but MS may present with many other typical MS presentations, including the following:
Aphasia or dysphasia
Hemianopsia
Seizures (5% of patients with MS)
Significant motor complaints without sensory deficits or dysautonomia (eg, bladder)
Physical: Classic MS findings on neurologic examination include the following:
Eye
Optic neuritis
Acutely, 50% of patients present with retrobulbar involvement; hence, funduscopy results are normal. "The patient sees nothing and the doctor sees nothing."
Anterior involvement causes papillitis, and differentiating this from papilledema is important. When inflammation involving the retina is extensive, look for presence of a macular star.
After several weeks, optic atrophy may be seen.
An afferent pupillary defect may be seen in the affected eye.
Visual acuity usually is impaired (ie, subtle to total blindness).
The classic finding is bilateral (unilateral much less common) internuclear ophthalmoplegia (INO), a lesion in the median longitudinal fasciculus (MLF) resulting in a weakness in adduction of the ipsilateral eye with nystagmus on abduction of the contralateral eye, an incomplete or slow abduction of the ipsilateral eye upon lateral gaze, with complete preservation of convergence.
Other eye findings include abnormal pupillary responses, acquired pendular nystagmus or sinusoidal involuntary oscillations of one or both eyes, and/or loss of smooth eye pursuit.
Regardless of the stage or classification, most authorities question the diagnosis of MS in a patient without at least one of these findings.
Spinal cord involvement
Acute transverse myelitis
Sphincter paralysis and unchanging level
Distinguish from Guillain-Barré syndrome
Paralysis, spasticity, and hyperreflexia are indicative of upper motor neuron dysfunction (ie, lateral corticospinal tracts). Decreased joint position and vibration sense (ie, dorsal columns) are common findings.
Decreased pain and temperature (ie, lateral spinothalamic tracts) are less common. The sparing of these symptoms may be diagnostically helpful.
The degree of corticospinal tract findings tends to correlate with bladder, bowel, and sexual dysautonomias.
Cerebellar findings: Disequilibrium, truncal or limb ataxia, scanning (ie, monotonous) speech, intention tremor, and saccadic dysmetria are common cerebellar findings.
Lhermitte sign: Neck flexion results in an electric shocklike feeling in the torso or extremities
Acute disseminated encephalitis
Most commonly, altered mental status and/or personality changes
Focal findings (eg, cranial nerve defects, hemiparesis, focal seizures, autonomic dysfunction)
Cranial nerve defects
Ataxia
Dysphasia
Meningismus, usually less common and pronounced than in meningitis
Unusual findings in MS include the absence of eye findings and isolated motor, sensory, cerebellar, and cranial nerve lesions.
Causes: MS commonly is believed to result from an autoimmune process. What triggers the autoimmune process is not clear, but the nonrandom nature of its geographic distribution suggests an isolated or additive environmental effect and/or inadvertent activation and dysregulation of CNS immune processes by a retroviral infection that was perhaps acquired in childhood. On the basis of bench research findings, some authorities implicate human herpesvirus-6 (HHV-6) variant B group 2, while others implicate Chlamydia pneumonia.
Polygene inheritance accounts for a familial rate of 10-20%; yet, most studies confirm that a monozygotic twin has only a 30% risk of acquiring MS, suggesting a genetic predisposition to an environmental viral agent.
As in systemic lupus erythematosus (SLE), human leukocyte antigen (HLA) patterns of patients with MS tend to differ from those of the general population.
Optic neuritis is attributable to MS in 50% of cases; the remaining 50% of cases are probably postinfectious. Ischemic optic neuropathy, arteriovenous malformations, tumors, and other compressive lesions usually present more gradually with additional symptoms or atypical features, but these complications should be pursued aggressively in any patient presenting with ON.
Acute transverse myelitis, when not attributable to MS, most likely is infectious (eg, Epstein-Barr virus [EBV], Lyme [rare]) or postinfectious. An important ED exclusion in these patients is mechanical compression by tumor, abscess, or aneurysm.
Acute disseminated encephalitis involves a poorly defined immune-mediated demyelinating process.
Classic MS symptoms
Sensory loss (ie, paresthesias) usually is an early complaint.
Motor (eg, muscle cramping secondary to spasticity) and autonomic (eg, bladder, bowel, sexual dysfunction) spinal cord symptoms may be present.
Cerebellar symptoms (eg, Charcot triad of dysarthria, ataxia, tremor) may occur.
Constitutional symptoms, especially fatigue (which occurs in 70% of cases) and dizziness, may be present.
Subjective difficulties with attention span, concentration, memory, and judgment may be noted any time during the disease course.
About 50% of patients with MS have impairment, usually mild, in information processing on neuropsychological testing.
Depression is common, but euphoria is less common.
Over the course of the disease, 5-10% of patients develop an overt psychiatric disorder (eg, manic depression, paranoia, major depression) or dementia.
Eye symptoms, including diplopia on lateral gaze, occur in 33% of patients.
Trigeminal neuralgia may occur.
Optic neuritis (ON) (ie, inflammation or demyelination of optic nerve) is the initial presentation of 15% of patients with MS. Fifty percent of all patients who present with ON have MS. Isolated episodes of ON, even if they are recurrent, do not represent MS.
Acute onset (ie, occurring over minutes or hours, rarely days) of single eye visual blurring, decreased acuity (ie, usually scotoma), decreased color perception, and/or discomfort of the moving eye(s) are symptoms that are indicative of ON.
The 3 phenomena associated with ON or compressive/ischemic neuritis are as follows:
Phosphenes, or flashes of light, usually are precipitated by eye movements.
Uhthoff phenomenon or deterioration of vision is induced by exercise, a hot meal, or a hot bath.
The Pulfrich effect occurs when latencies between the eyes are unequal, resulting in a sense of disorientation in moving traffic.
Acute transverse myelitis
Partial acute transverse myelitis, rather than total, usually is a manifestation of MS. Strongly consider mechanical compression in the differential diagnosis.
Acute partial loss of motor, sensory, autonomic, reflex, and sphincter function below the level of the lesion indicates acute transverse myelitis.
Devic syndrome is acute transverse myelitis accompanied by bilateral ON.
Acute disseminated encephalitis is pathophysiologically and radiographically identical to MS. It is characterized by acute onset of motor, sensory, cerebellar, and cranial nerve dysfunction with encephalopathy, progressing to coma and eventual death in 30% of such cases.
MS as a sole symptom is unusual, but MS may present with many other typical MS presentations, including the following:
Aphasia or dysphasia
Hemianopsia
Seizures (5% of patients with MS)
Significant motor complaints without sensory deficits or dysautonomia (eg, bladder)
Physical: Classic MS findings on neurologic examination include the following:
Eye
Optic neuritis
Acutely, 50% of patients present with retrobulbar involvement; hence, funduscopy results are normal. "The patient sees nothing and the doctor sees nothing."
Anterior involvement causes papillitis, and differentiating this from papilledema is important. When inflammation involving the retina is extensive, look for presence of a macular star.
After several weeks, optic atrophy may be seen.
An afferent pupillary defect may be seen in the affected eye.
Visual acuity usually is impaired (ie, subtle to total blindness).
The classic finding is bilateral (unilateral much less common) internuclear ophthalmoplegia (INO), a lesion in the median longitudinal fasciculus (MLF) resulting in a weakness in adduction of the ipsilateral eye with nystagmus on abduction of the contralateral eye, an incomplete or slow abduction of the ipsilateral eye upon lateral gaze, with complete preservation of convergence.
Other eye findings include abnormal pupillary responses, acquired pendular nystagmus or sinusoidal involuntary oscillations of one or both eyes, and/or loss of smooth eye pursuit.
Regardless of the stage or classification, most authorities question the diagnosis of MS in a patient without at least one of these findings.
Spinal cord involvement
Acute transverse myelitis
Sphincter paralysis and unchanging level
Distinguish from Guillain-Barré syndrome
Paralysis, spasticity, and hyperreflexia are indicative of upper motor neuron dysfunction (ie, lateral corticospinal tracts). Decreased joint position and vibration sense (ie, dorsal columns) are common findings.
Decreased pain and temperature (ie, lateral spinothalamic tracts) are less common. The sparing of these symptoms may be diagnostically helpful.
The degree of corticospinal tract findings tends to correlate with bladder, bowel, and sexual dysautonomias.
Cerebellar findings: Disequilibrium, truncal or limb ataxia, scanning (ie, monotonous) speech, intention tremor, and saccadic dysmetria are common cerebellar findings.
Lhermitte sign: Neck flexion results in an electric shocklike feeling in the torso or extremities
Acute disseminated encephalitis
Most commonly, altered mental status and/or personality changes
Focal findings (eg, cranial nerve defects, hemiparesis, focal seizures, autonomic dysfunction)
Cranial nerve defects
Ataxia
Dysphasia
Meningismus, usually less common and pronounced than in meningitis
Unusual findings in MS include the absence of eye findings and isolated motor, sensory, cerebellar, and cranial nerve lesions.
Causes: MS commonly is believed to result from an autoimmune process. What triggers the autoimmune process is not clear, but the nonrandom nature of its geographic distribution suggests an isolated or additive environmental effect and/or inadvertent activation and dysregulation of CNS immune processes by a retroviral infection that was perhaps acquired in childhood. On the basis of bench research findings, some authorities implicate human herpesvirus-6 (HHV-6) variant B group 2, while others implicate Chlamydia pneumonia.
Polygene inheritance accounts for a familial rate of 10-20%; yet, most studies confirm that a monozygotic twin has only a 30% risk of acquiring MS, suggesting a genetic predisposition to an environmental viral agent.
As in systemic lupus erythematosus (SLE), human leukocyte antigen (HLA) patterns of patients with MS tend to differ from those of the general population.
Optic neuritis is attributable to MS in 50% of cases; the remaining 50% of cases are probably postinfectious. Ischemic optic neuropathy, arteriovenous malformations, tumors, and other compressive lesions usually present more gradually with additional symptoms or atypical features, but these complications should be pursued aggressively in any patient presenting with ON.
Acute transverse myelitis, when not attributable to MS, most likely is infectious (eg, Epstein-Barr virus [EBV], Lyme [rare]) or postinfectious. An important ED exclusion in these patients is mechanical compression by tumor, abscess, or aneurysm.
Acute disseminated encephalitis involves a poorly defined immune-mediated demyelinating process.