DYSPHASIA typical MS presentations

[Guest guest]

They told me at my Physical Therapy visits that I would need a " Speech

therapists " for the " swallowing problem " with my MS.

I had no idea it would be a Speech therapists! But it is.

They are talking about setting it up for me. I don't look forward to yet

ANOTHER " thing " to have to do!

Elf

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.

Although no present studies support a connection between hepatitis B

vaccination and MS, worldwide anecdotal reports prompted the Centers for

Disease Control and Prevention (CDC) to investigate this possibility

(see CDC web site

http://www.cdc.gov/nip/vacsafe/concerns/MS/default.htm).

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.