Signs and symptoms of multiple sclerosis: Difference between revisions
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==Internuclear ophthalmoplegia== |
==Internuclear ophthalmoplegia== |
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{{Main|Internuclear ophthalmoplegia}} |
{{Main|Internuclear ophthalmoplegia}} |
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It is a disorder of conjugate lateral gaze. The affected eye shows impairment of [[adduction]]. The partner eye diverges from the affected eye during abduction, producing [[diplopia]]; during extreme abduction, compensatory [[nystagmus]] can be seen in the partner eye. |
It is a disorder of conjugate lateral gaze. The affected eye shows impairment of [[adduction]]. The partner eye diverges from the affected eye during abduction, producing [[diplopia]]; during extreme abduction, compensatory [[nystagmus]] can be seen in the partner eye. Diplopia means double vision while nystagmus is involuntary [[eye movement]]characterized by alternating [[smooth pursuit]] in one direction and a [[saccadic movement]] in the other direction. |
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Internuclear ophthalmoplegia occurs when MS affects a part of the [[brain stem]] called the [[medial longitudinal fasciculus]], which is responsible for communication between the two eyes by connecting the [[abducens nucleus]] of one side to the [[occulomotor nucleus]] of the opposite side.. This results in the failure of the [[medial rectus muscle]] to contract appropriately, so that the eyes do not move equally (called disconjugate gaze). |
Internuclear ophthalmoplegia occurs when MS affects a part of the [[brain stem]] called the [[medial longitudinal fasciculus]], which is responsible for communication between the two eyes by connecting the [[abducens nucleus]] of one side to the [[occulomotor nucleus]] of the opposite side.. This results in the failure of the [[medial rectus muscle]] to contract appropriately, so that the eyes do not move equally (called disconjugate gaze). |
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Different drugs as well as optic compensatory systems and prisms can be used to improve this symptoms.;<ref>{{cite journal |author=Leigh RJ, Averbuch-Heller L, Tomsak RL, Remler BF, Yaniglos SS, Dell'Osso LF |title=Treatment of abnormal eye movements that impair vision: strategies based on current concepts of physiology and pharmacology |journal=Ann. Neurol. |volume=36 |issue=2 |pages=129-41 |year=1994 |pmid=8053648}}</ref><ref> {{cite journal |author=Starck M, Albrecht H, Pöllmann W, Straube A, Dieterich M |title=Drug therapy for acquired pendular nystagmus in multiple sclerosis |journal=J. Neurol. |volume=244 |issue=1 |pages=9-16 |year=1997 |pmid=9007739}}</ref><ref>{{cite journal |author=Clanet MG, Brassat D |title=The management of multiple sclerosis patients |journal=Curr. Opin. Neurol. |volume=13 |issue=3 |pages=263-70 |year=2000 |pmid=10871249}}</ref><ref>{{cite journal |author=Menon GJ, Thaller VT |title=Therapeutic external ophthalmoplegia with bilateral retrobulbar botulinum toxin- an effective treatment for acquired nystagmus with oscillopsia |journal=Eye (London, England) |volume=16 |issue=6 |pages=804-6 |year=2002 |pmid=12439689}}</ref> |
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Surgery can also be used in some cases.<ref>{{cite journal |author=Menon GJ, Thaller VT |title=Therapeutic external ophthalmoplegia with bilateral retrobulbar botulinum toxin- an effective treatment for acquired nystagmus with oscillopsia |journal=Eye (London, England) |volume=16 |issue=6 |pages=804-6 |year=2002 |pmid=12439689}}</ref> |
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==Transverse myelitis== |
==Transverse myelitis== |
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Revision as of 09:07, 6 May 2007
MS can cause a variety of symptoms, including changes in sensation (hypoesthesia), muscle weakness, abnormal muscle spasms, or difficulty to move; difficulties with coordination and balance; problems in speech (Dysarthria) or swallowing (Dysphagia), visual problems (Nystagmus, optic neuritis, or diplopia), fatigue and acute or chronic pain syndromes, bladder and bowel difficulties, cognitive impairment, or emotional symptomatology (mainly depression).
The initial attacks are often transient, mild (or asymptomatic), and self-limited. They often do not prompt a health care visit and sometimes are only identified in retrospect once the diagnosis has been made based on further attacks. The most common initial symptoms reported are: changes in sensation in the arms, legs or face (33%), complete or partial vision loss (optic neuritis) (20%), weakness (13%), double vision (7%), unsteadiness when walking (5%), and balance problems (3%); but many rare initial symptoms have been reported such as aphasia or psychosis.[1][2] Fifteen percent of individuals have multiple symptoms when they first seek medical attention.[3] For some people the initial MS attack is preceded by infection, trauma, or strenuous physical effort.
Cognitive
Cognitive impairments are common. Neuropsychological studies suggest that 40 to 60 percent of patients have cognitive deficits;[4] with the lowest percentages usually from community-based studies and the highest ones from hospital-based.
Cognitive impairment, sometimes referred to as brain fog, is already present in the beginnings of the disease.[5] Even in probable MS (after the first attack but before a second confirmatory one) up to 50% of patients have mild impairment.[6]
Some of the most common declines are in recent memory, attention, processing speed, visual-spatial abilities and executive functions.[7] Other cognitive-related symptoms are emotional instability, and fatigue, including purely neurological fatigue. The cognitive impairments in MS are usually mild; and only in 5% of patients can we speak of dementia. Nevertheless they are related with unemployment and reduced social interactions.[8] They are also related with driving difficulties.[9]
Emotional
Emotional symptoms are also common and are thought to be both the normal response to having a debilitating disease and the result of damage to specific areas of the cental nervous system that generate and control emotions.
Clinical depression is the most common neuropsychiatric condition: lifetime depression prevalence rates of 40-50% and 12 month prevalence rates around 20% have been typically reported for samples of people with MS; being these figures considerably higher than those reported for sane people or with other chronic illnesses.[10][11] Many brain-imaging studies have tried to relate depression to lesions in different brain regions with variable success. On balance the evidence seems to favour an association with neuropathology in the left anterior temporal/parietal regions.[12]
Other feelings such as anger, anxiety, frustration, and hopelessness also appear frequently, and suicide is a very real threat since 15% of deaths in MS sufferers are due to this cause.[13]
Optic neuritis
Some individuals experience rapid onset of pain in one eye, followed by blurry vision in part or all of the visual field of that eye. Inflammation of the optic nerve causes loss of vision usually due to the swelling and destruction of the myelin sheath covering the optic nerve.
The blurred vision usually resolves within ten weeks, but individuals are often left with less vivid color vision (especially red) in the affected eye.
Up to 50% of patients with MS will develop an episode of optic neuritis, and 20% of the time optic neuritis is the presenting sign of MS. The presence of demyelinating white matter lesions on brain MRI at the time of presentation of optic neuritis is the strongest predictor for developing clinically definite MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis. At five years follow-up, the overall risk of developing MS is 30%, with or without MRI lesions. Patients with a normal MRI still develop MS (16%), but at a lower rate compared to those patients with three or more MRI lesions (51%). From the other perspective, however, almost half (44%) of patients with any demyelinating lesions on MRI at presentation will not have developed MS ten years later. [14][15]
Systemic intravenous treatment with corticosteroids, which may quicken the healing of the optic nerve, prevent complete loss of vision, and delay the onset of other symptoms, is often recommended.
Internuclear ophthalmoplegia
It is a disorder of conjugate lateral gaze. The affected eye shows impairment of adduction. The partner eye diverges from the affected eye during abduction, producing diplopia; during extreme abduction, compensatory nystagmus can be seen in the partner eye. Diplopia means double vision while nystagmus is involuntary eye movementcharacterized by alternating smooth pursuit in one direction and a saccadic movement in the other direction.
Internuclear ophthalmoplegia occurs when MS affects a part of the brain stem called the medial longitudinal fasciculus, which is responsible for communication between the two eyes by connecting the abducens nucleus of one side to the occulomotor nucleus of the opposite side.. This results in the failure of the medial rectus muscle to contract appropriately, so that the eyes do not move equally (called disconjugate gaze).
Different drugs as well as optic compensatory systems and prisms can be used to improve this symptoms.;[16][17][18][19] Surgery can also be used in some cases.[20]
Transverse myelitis
Some MS patients develop rapid onset of numbness, weakness, bowel or bladder dysfunction, and/or loss of muscle function, typically in the lower half of the body. This is the result of MS attacking the spinal cord. As many as 80% of individuals with transverse myelitis are left with lasting disabilities, even though there is usually some improvement during the first two years.
References
- ^ Navarro S, Mondéjar-Marín B, Pedrosa-Guerrero A, Pérez-Molina I, Garrido-Robres J, Alvarez-Tejerina A. "[Aphasia and parietal syndrome as the presenting symptoms of a demyelinating disease with pseudotumoral lesions]". Rev Neurol. 41 (10): 601–3. PMID 16288423.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Jongen P (2006). "Psychiatric onset of multiple sclerosis". J Neurol Sci. 245 (1–2): 59–62. PMID 16631798.
- ^ Paty D, Studney D, Redekop K, Lublin F. MS COSTAR: a computerized patient record adapted for clinical research purposes. Ann Neurol 1994;36 Suppl:S134-5. PMID 8017875
- ^ Rao S, Leo G, Bernardin L, Unverzagt F (1991). "Cognitive dysfunction in multiple sclerosis. I. Frequency, patterns, and prediction". Neurology. 41 (5): 685–91. PMID 2027484.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ "Attention impairment in recently diagnosed multiple sclerosis". Eur J Neurol. 5 (1): 61–66. 1998. PMID 10210813.
- ^ Achiron A, Barak Y (2003). "Cognitive impairment in probable multiple sclerosis". J Neurol Neurosurg Psychiatry. 74 (4): 443–6. PMID 12640060.
- ^ Bobholz J, Rao S (2003). "Cognitive dysfunction in multiple sclerosis: a review of recent developments". Curr Opin Neurol. 16 (3): 283–8. PMID 12858063.
- ^ Amato M, Ponziani G, Siracusa G, Sorbi S (2001). "Cognitive dysfunction in early-onset multiple sclerosis: a reappraisal after 10 years". Arch Neurol. 58 (10): 1602–6. PMID 11594918.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Shawaryn M, Schultheis M, Garay E, Deluca J (2002). "Assessing functional status: exploring the relationship between the multiple sclerosis functional composite and driving". Arch Phys Med Rehabil. 83 (8): 1123–9. PMID 12161835.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Sadovnick A, Remick R, Allen J, Swartz E, Yee I, Eisen K, Farquhar R, Hashimoto S, Hooge J, Kastrukoff L, Morrison W, Nelson J, Oger J, Paty D (1996). "Depression and multiple sclerosis". Neurology. 46 (3): 628–32. PMID 8618657.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Patten S, Beck C, Williams J, Barbui C, Metz L (2003). "Major depression in multiple sclerosis: a population-based perspective". Neurology. 61 (11): 1524–7. PMID 14663036.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Siegert R, Abernethy D (2005). "Depression in multiple sclerosis: a review". J. Neurol. Neurosurg. Psychiatr. 76 (4): 469–75. PMID 15774430.
- ^ Sadovnick A, Eisen K, Ebers G, Paty D (1991). "Cause of death in patients attending multiple sclerosis clinics". Neurology. 41 (8): 1193–6. PMID 1866003.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Beck RW, Trobe JD (1995). "What we have learned from the Optic Neuritis Treatment Trial". Ophthalmology. 102 (10): 1504–8. PMID 9097798.
- ^ "The 5-year risk of MS after optic neuritis: experience of the optic neuritis treatment trial. 1997". Neurology. 57 (12 Suppl 5): S36-45. 2001. PMID 11902594.
- ^ Leigh RJ, Averbuch-Heller L, Tomsak RL, Remler BF, Yaniglos SS, Dell'Osso LF (1994). "Treatment of abnormal eye movements that impair vision: strategies based on current concepts of physiology and pharmacology". Ann. Neurol. 36 (2): 129–41. PMID 8053648.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Starck M, Albrecht H, Pöllmann W, Straube A, Dieterich M (1997). "Drug therapy for acquired pendular nystagmus in multiple sclerosis". J. Neurol. 244 (1): 9–16. PMID 9007739.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Clanet MG, Brassat D (2000). "The management of multiple sclerosis patients". Curr. Opin. Neurol. 13 (3): 263–70. PMID 10871249.
- ^ Menon GJ, Thaller VT (2002). "Therapeutic external ophthalmoplegia with bilateral retrobulbar botulinum toxin- an effective treatment for acquired nystagmus with oscillopsia". Eye (London, England). 16 (6): 804–6. PMID 12439689.
- ^ Menon GJ, Thaller VT (2002). "Therapeutic external ophthalmoplegia with bilateral retrobulbar botulinum toxin- an effective treatment for acquired nystagmus with oscillopsia". Eye (London, England). 16 (6): 804–6. PMID 12439689.