Wikia

Psychology Wiki

Multiple sclerosis signs and symptoms

Talk0
34,142pages on
this wiki
Revision as of 19:23, November 24, 2008 by Dr Joe Kiff (Talk | contribs)

(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·


Multiple sclerosis can cause a variety of symptoms, including paranoid delusions, 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 major depression). The main clinical measure of disability progression and severity of the symptoms is the Expanded Disability Status Scale or EDSS.[1]

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.[2][3] Fifteen percent of individuals have multiple symptoms when they first seek medical attention.[4] For some people the initial MS attack is preceded by infection, trauma, or strenuous physical effort.

BladderEdit

Bladder problems (See also urinary system and urination) appear in 70-80% of MS patients and they have an important effect both in hygiene habits and social activity.[5][6] However bladder problems are usually related with high levels of disability and pyramidal signs in lower limbs[7]

The most common problems are an increase of frequency and urgency (incontinence) but difficulties to begin urination, hesitation, leaking, retention and sensation of incomplete urination also appear. When there is retention secondary urinary infections are common.

There are many cortical and subcortical structures implicated in micturition.[8] Accordingly; MS lesions in different central nervous system structures can cause these kind of symptoms.

Treatment objectives are alleviation of symptoms of urinary dysfunction, treatment of urinary infections, reduction of complicating factors and preservation of renal function.Treatments can be classified in two main subtypes: pharmacological and non pharmacological. Pharmacological treatments vary greatly depending on the origin or type of dysfunction; however some examples of the medications used are:[9] alfuzosin for retention,[10] trospium and flavoxate for urgency and incontinency,[11][12] or desmopressin for nocturia.[13][14] Non pharmacological treatments involve the use of pelvic floor muscle training, stimulation, biofeedback, pessaries, bladder retraining, and sometimes intermittent catheterization.[15]

CognitiveEdit

Cognitive impairments are common. Neuropsychological studies suggest that 40 to 60 percent of patients have cognitive deficits;[16] 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.[17] Even in probable MS (after the first attack but before a second confirmatory one) up to 50% of patients have mild impairment.[18]

Some of the most common declines are in recent memory, attention, processing speed, visual-spatial abilities and executive functions.[19] 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.[20] They are also related with driving difficulties.[21]

Neurocognitive testing is important for determining the extent of cognitive deficits. Neuropsychological stimulation may help to reverse or decrease the cognitive defects although its management relies on lifestyle strategies.Interferons have demonstrated that can help to reduce cognitive limitations in multiple sclerosis.[22] Anticholinesterase drugs such as donepezil commonly used in alzheimer disease; although not approved yet for multiple sclerosis; have also shown efficacy in different clinical trials.[23][24][25]

EmotionalEdit

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 central 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; these figures are considerably higher than those for the general population or for people with other chronic illnesses.[26][27] 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.[28]

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.[29]

FatigueEdit

Fatigue is very common and disabling in MS. At the same time it has a close relationship with depressive symptomatology.[30] When depression is reduced fatigue also tends to improve, so patients should be evaluated for depression before other therapeutic approaches are used.[31]. In a similar way other factors like disturbed sleep, chronic pain, poor nutrition, or even some medications can contribute to fatigue; and therefore medical professionals are encouraged to identify and modify them.[32] There are also different medications used to treat fatigue; such as amantadine,[33][34] or pemoline;[35][36] as well as psychological interventions of energy conservation;[37][38] but the effects of all of them are small. For this reason fatigue is a very difficult symptom to manage. Fatigue has been related to specific brain areas in MS using magnetic resonance imaging.[39]

Internuclear ophthalmoplegiaEdit

File:Internuclear ophthalmoplegia.jpg
Main article: Internuclear ophthalmoplegia

Internuclear ophthalmoplegia 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.

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 oculomotor 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.[40][41][42][43] Surgery can also be used in some cases for this problem.[44]

Mobility restrictionsEdit

Restrictions in mobility (walking, transfers, bed mobility) are common in individuals suffering from multiple sclerosis. Within 10 years after the onset of MS one-third of patients reach a score of 6 on the Expanded Disability Status Scale (requiring the use of a unilateral walking aid),and by 30 years the proportion increases to 83%. Within 5 years the Expanded Disability Status Score is 6 in 50% of those with the progressive form of MS.[45]

In MS a wide range of impairments may exist which can act either alone or in combination to impact directly on a person's balance, function and mobility. Such impairments include fatigue, weakness, hypertonicity, low exercise tolerance, impaired balance, ataxia and tremor.[46]

Interventions may be aimed at the level of the impairments that reduce mobility; or at the level of disability. At this second level interventions include provision, education and instruction in use of equipment such as walking aids, wheelchairs, motorized scooters and car adaptations; and instruction about compensatory strategies to accomplish an activity, (for example,undertaking safe transfers by pivoting in a flexed posture rather than standing up and stepping around)

Optic neuritisEdit

Main article: Optic neuritis

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. [47][48]

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 because of 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.

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.

PainEdit

Pain is a common symptom in MS; appearing in 55% of patients at some point of their disease process; specially as time passes.[49] It is strong and debilitating and has a profound effect in the quality of life and mental health of the sufferer.[50] It usually appears after a lesion to the ascending or descending tracts that control the transmission of painful stimulus. such as the anterolateral system, but many other causes are also possible.[51] Most frequent pains reported are headaches (40%), dysesthetic limb pain (19%), back pain (17%), and painful spasms (11%).[52]

Acute pain is mainly due to optic neuritis, being corticosteroids the best treatment available; to trigeminal neuralgia, to Lhermitte's sign or to dysesthesias.[53] Subacute pain is usually secondary to the disease and can be consequence of being too much time in the same position, urinary retention, infected skin ulcers and many others. Treatment will depend on cause. Chronic pain is very common and the harder to treat being its most common cause dysesthesias.

Trigeminal neuralgiaEdit

Trigeminal neuralgia or "tic douloureux", is a disorder of the trigeminal nerve that causes episodes of intense pain in the eyes, lips, nose, scalp, forehead, and jaw. It affects 1 to 2% of MS patients during their disease.[54][55] The episodes of pain occur paroxysmally, or suddenly; and the patients describe it as trigger area on the face, so sensitive that touching or even air currents can bring an episode of pain. Usually it's successfully treated with anticonvulsants such as carbamazepine[56] or phenytoin[57] but others such as gabapentin[58] can be used. [59] When drugs are not effective enough surgery may be recommended. Further damage to the nerve to prevent the transmission of pain (Rhyzotomy) has proven its efficacy;[60] however the beneficial effects and risks in multiple sclerosis patients of those procedures that consist in relieving the pressure on the nerve are still under discussion.[61][62]

Lhermitte's signEdit

Lhermitte's sign is an electrical sensation that runs down the back and into the limbs, and is produced by bending the neck forward. The sign suggests a lesion of the dorsal columns of the cervical cord or of the caudal medulla; correlating significantly with cervical MRI abnormalities.[63] Between 25 and 40% of MS patients report having Lhermitte's sign during the course of their illness. [64][65][66]

DysesthesiasEdit

Dysesthesias are disagreeable sensations produced by ordinary stimuli. The abnormal sensations are often described as painful feelings such as burning, wetness, itching, electric shock or pins and needles; and are caused by lesions of the peripheral or central sensory pathways. Both Lhermitte's sign and painful dysesthesias usually respond well to treatment with carbamazepine, clonazepam or amitriptyline. [67][68][69]

SexualEdit

Sexual dysfunction (SD) is one of many symptoms affecting persons with a diagnosis of multiple sclerosis (MS) and other neurological disease. SD in men encompasses both erectile and ejaculatory disorder. The prevalence of SD in men with MS ranges from 75 to 91% (O'Leary et al., 2007). Erectile dysfunction appears to be the most common form of SD documented in MS. SD may be due to alteration of the ejaculatory reflexe which may be affected by neurological conditions such as MS [70]

SpasticityEdit

Spasticity is characterised by increased stiffness and slowness in limb movement, the development of certain postures, an association with weakness of voluntary muscle power, and with involuntary and sometimes painful spasms of limbs.[32] A physiotherapist can help to reduce spasticity and avoid the development of contractures with techniques such as passive stretching.[71] There is evidence, albeit limited, of the clinical effectiveness of baclofen,[72] dantrolene,[73] diazepam,[74] and tizanidine.[75][76][77] In the most complicated cases intrathecal injections of baclofen can be used.[78] There are also palliative measures like castings, splints or customised seatings.[32]

Transverse myelitisEdit

Main article: 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. The symptoms and signs depend upon the level of the spinal cord involved and the extent of the involvement.

Prognosis for complete recovery is generally poor. Recovery from transverse myelitis usually begins between weeks 2 and 12 following onset and may continue for up to 2 years in some patients and as many as 80% of individuals with transverse myelitis are left with lasting disabilities.[How to reference and link to summary or text]

Treatment is usually symptomatic only, corticosteroids being used with limited success.

Tremor and ataxiaEdit

Main article: Tremor

Tremor is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro movements (oscillations) of one or more parts of the body. It is the most common of all involuntary movements and can affect the hands, arms, head, face, vocal cords, trunk, and legs. Ataxia is an unsteady and clumsy motion of the limbs or torso due to a failure of the gross coordination of muscle movements. People with ataxia experience a failure of muscle control in their arms and legs, resulting in a lack of balance and coordination or a disturbance of gait.

Tremor and ataxia are frequent in MS. They present in 25 to 60% of patients. They can be very disabling and embarrassing, and are difficult to manage.[79] The origin of tremor in MS is difficult to precise but it can be due to a mixture of different factors such as damage to the cerebellar connections, weakness, spasticity, etc.

In the treatment of tremor many medications have been proposed; however their efficacy is very limited. Medications that have been reported to provide some relief are isoniazid,[80][81][82][83] carbamazepine,[84] propranolol;[85][86][87] and gluthetimide,[88] but published evidence of effectiveness is very limited.[89] Physical therapy is not indicated as a treatment for tremor or ataxia; however, the use of different orthese devices can help. An example is the use of wrist bandages with weights, which can be useful to increase the inertia of movement and therefore reduce tremor.[90] Daily use objects have also to be adapted so they are easier to grab and use.

If all these measures fail some patients are candidates for thalamus surgery. This kind of surgery can be both a thalamotomy or the implantation of a thalamic stimulator. Complications are frequent (30% in thalamotomy and 10% in deep brain stimulation) and include a worsening of ataxia, dysarthria and hemiparesis. Thalamotomy is a more efficacious surgical treatment for intractable MS tremor, however the higher incidence of persistent neurological deficits in patients receiving lesional surgery supports the use of deep brain stimulation as the preferred surgical strategy.[91]

ReferencesEdit

  1. Kurtzke JF (1983). Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology 33 (11): 1444–52.
  2. 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.
  3. Jongen P (2006). Psychiatric onset of multiple sclerosis. J Neurol Sci 245 (1-2): 59–62.
  4. 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
  5. Hennessey A, Robertson NP, Swingler R, Compston DA (1999). Urinary, faecal and sexual dysfunction in patients with multiple sclerosis. J. Neurol. 246 (11): 1027–32.
  6. Burguera-Hernández JA (2000). [Urinary alterations in multiple sclerosis]. Revista de neurologia 30 (10): 989–92.
  7. Betts CD, D'Mellow MT, Fowler CJ (1993). Urinary symptoms and the neurological features of bladder dysfunction in multiple sclerosis. J. Neurol. Neurosurg. Psychiatr. 56 (3): 245–50.
  8. Nour S, Svarer C, Kristensen JK, Paulson OB, Law I (2000). Cerebral activation during micturition in normal men. Brain 123 ( Pt 4): 781–9.
  9. Ayuso-Peralta L, de Andrés C (2002). [Symptomatic treatment of multiple sclerosis]. Revista de neurologia 35 (12): 1141–53.
  10. Information from the USA National library of medicine on alfuzosin [1]
  11. Information from the USA National library of medicine on trospium [2]
  12. Information from the USA National library of medicine on flavoxate [3]
  13. Bosma R, Wynia K, Havlíková E, De Keyser J, Middel B (2005). Efficacy of desmopressin in patients with multiple sclerosis suffering from bladder dysfunction: a meta-analysis. Acta Neurol. Scand. 112 (1): 1–5.
  14. Information from the USA National library of medicine on desmopressin [4]
  15. Frances M Diro (2006) "Urological Management in Neurological Disease". [5]
  16. Rao S, Leo G, Bernardin L, Unverzagt F (1991). Cognitive dysfunction in multiple sclerosis. I. Frequency, patterns, and prediction. Neurology 41 (5): 685–91.
  17. (1998) Attention impairment in recently diagnosed multiple sclerosis. Eur J Neurol 5 (1): 61–66.
  18. Achiron A, Barak Y (2003). Cognitive impairment in probable multiple sclerosis. J Neurol Neurosurg Psychiatry 74 (4): 443–6.
  19. Bobholz J, Rao S (2003). Cognitive dysfunction in multiple sclerosis: a review of recent developments. Curr Opin Neurol 16 (3): 283–8.
  20. 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.
  21. 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.
  22. Montalban X, Rio J (2006). Interferons and cognition. J Neurol Sci 245 (1-2): 137–40.
  23. Christodoulou C, Melville P, Scherl W, Macallister W, Elkins L, Krupp L (2006). Effects of donepezil on memory and cognition in multiple sclerosis. J Neurol Sci 245 (1-2): 127–36.
  24. Porcel J, Montalban X (2006). Anticholinesterasics in the treatment of cognitive impairment in multiple sclerosis. J Neurol Sci 245 (1-2): 177–81.
  25. Information from the USA National library of medicine on donepezil [6]
  26. 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.
  27. 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.
  28. Siegert R, Abernethy D (2005). Depression in multiple sclerosis: a review. J. Neurol. Neurosurg. Psychiatr. 76 (4): 469–75.
  29. Sadovnick A, Eisen K, Ebers G, Paty D (1991). Cause of death in patients attending multiple sclerosis clinics. Neurology 41 (8): 1193–6.
  30. Bakshi R (2003). Fatigue associated with multiple sclerosis: diagnosis, impact and management. Mult. Scler. 9 (3): 219–27.
  31. Mohr DC, Hart SL, Goldberg A (2003). Effects of treatment for depression on fatigue in multiple sclerosis. Psychosomatic medicine 65 (4): 542–7.
  32. 32.0 32.1 32.2 The Royal College of Physicians (2004). Multiple Sclerosis. National clinical guideline for diagnosis and management in primary and secondary care, Salisbury, Wiltshire: Sarum ColourView Group.Free full text (2004-08-13). Retrieved on 2007-10-01.
  33. Pucci E, Branãs P, D'Amico R, Giuliani G, Solari A, Taus C (2007). Amantadine for fatigue in multiple sclerosis. Cochrane database of systematic reviews (Online) (1): CD002818.
  34. Amantadine. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-07.
  35. Weinshenker BG, Penman M, Bass B, Ebers GC, Rice GP (1992). A double-blind, randomized, crossover trial of pemoline in fatigue associated with multiple sclerosis. Neurology 42 (8): 1468–71.
  36. Pemoline. US National Library of Medicine (Medline) (2006-01-01). Retrieved on 2007-10-07.
  37. Mathiowetz VG, Finlayson ML, Matuska KM, Chen HY, Luo P (2005). Randomized controlled trial of an energy conservation course for persons with multiple sclerosis. Mult. Scler. 11 (5): 592–601.
  38. Matuska K, Mathiowetz V, Finlayson M (2007). Use and perceived effectiveness of energy conservation strategies for managing multiple sclerosis fatigue. The American journal of occupational therapy. : official publication of the American Occupational Therapy Association 61 (1): 62–9.
  39. Sepulcre J, Masdeu J, Goñi J, et al (November 2008). Fatigue in multiple sclerosis is associated with the disruption of frontal and parietal pathways. Mult. Scler..
  40. 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.
  41. 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.
  42. Clanet MG, Brassat D (2000). The management of multiple sclerosis patients. Curr. Opin. Neurol. 13 (3): 263–70.
  43. 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.
  44. Jain S, Proudlock F, Constantinescu CS, Gottlob I (2002). Combined pharmacologic and surgical approach to acquired nystagmus due to multiple sclerosis. Am. J. Ophthalmol. 134 (5): 780–2.
  45. Weinshenker BG, Bass B, Rice GP, et al (1989). The natural history of multiple sclerosis: a geographically based study. I. Clinical course and disability. Brain 112 ( Pt 1): 133–46.
  46. Freeman JA (2001). Improving mobility and functional independence in persons with multiple sclerosis. J. Neurol. 248 (4): 255–9.
  47. Beck RW, Trobe JD (1995). What we have learned from the Optic Neuritis Treatment Trial. Ophthalmology 102 (10): 1504–8.
  48. (2001) The 5-year risk of MS after optic neuritis: experience of the optic neuritis treatment trial. 1997. Neurology 57 (12 Suppl 5): S36–45.
  49. Stenager E, Knudsen L, Jensen K (1995). Acute and chronic pain syndromes in multiple sclerosis. A 5-year follow-up study. Italian journal of neurological sciences 16 (9): 629–32.
  50. Archibald CJ, McGrath PJ, Ritvo PG, et al (1994). Pain prevalence, severity and impact in a clinic sample of multiple sclerosis patients. Pain 58 (1): 89–93.
  51. Clanet MG, Brassat D (2000). The management of multiple sclerosis patients. Curr. Opin. Neurol. 13 (3): 263–70.
  52. Pöllmann W, Feneberg W, Erasmus LP (2004). [Pain in multiple sclerosis--a still underestimated problem. The 1 year prevalence of pain syndromes, significance and quality of care of multiple sclerosis inpatients]. Der Nervenarzt 75 (2): 135–40.
  53. Kerns RD, Kassirer M, Otis J (2002). Pain in multiple sclerosis: a biopsychosocial perspective. Journal of rehabilitation research and development 39 (2): 225–32.
  54. Brisman R (1987). Trigeminal neuralgia and multiple sclerosis. Arch. Neurol. 44 (4): 379–81.
  55. Bayer DB, Stenger TG (1979). Trigeminal neuralgia: an overview. Oral Surg. Oral Med. Oral Pathol. 48 (5): 393–9.
  56. Information from the USA National library of medicine on carbamazepine [7]
  57. Information from the USA National library of medicine on phenytoin [8]
  58. Information from the USA National library of medicine on gabapentin [9]
  59. Solaro C, Messmer Uccelli M, Uccelli A, Leandri M, Mancardi GL (2000). Low-dose gabapentin combined with either lamotrigine or carbamazepine can be useful therapies for trigeminal neuralgia in multiple sclerosis. Eur. Neurol. 44 (1): 45–8.
  60. Kondziolka D, Lunsford LD, Bissonette DJ (1994). Long-term results after glycerol rhizotomy for multiple sclerosis-related trigeminal neuralgia. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 21 (2): 137–40.
  61. Athanasiou TC, Patel NK, Renowden SA, Coakham HB (2005). Some patients with multiple sclerosis have neurovascular compression causing their trigeminal neuralgia and can be treated effectively with MVD: report of five cases. British journal of neurosurgery 19 (6): 463–8.
  62. Eldridge PR, Sinha AK, Javadpour M, Littlechild P, Varma TR (2003). Microvascular decompression for trigeminal neuralgia in patients with multiple sclerosis. Stereotactic and functional neurosurgery 81 (1-4): 57–64.
  63. Gutrecht JA, Zamani AA, Slagado ED (1993). Anatomic-radiologic basis of Lhermitte's sign in multiple sclerosis. Arch. Neurol. 50 (8): 849–51.
  64. Al-Araji AH, Oger J (2005). Reappraisal of Lhermitte's sign in multiple sclerosis. Mult. Scler. 11 (4): 398–402.
  65. Sandyk R, Dann LC (1995). Resolution of Lhermitte's sign in multiple sclerosis by treatment with weak electromagnetic fields. Int. J. Neurosci. 81 (3-4): 215–24.
  66. Kanchandani R, Howe JG (1982). Lhermitte's sign in multiple sclerosis: a clinical survey and review of the literature. J. Neurol. Neurosurg. Psychiatr. 45 (4): 308–12.
  67. Information from the USA National library of medicine on clonazepam[10]
  68. Information from the USA National library of medicine on amitriptyline[11]
  69. Moulin DE, Foley KM, Ebers GC (1988). Pain syndromes in multiple sclerosis. Neurology 38 (12): 1830–4.
  70. O'Leary, M., Heyman, R., Erickson, J., Chancellor, M.B.: Premature ejaculation and MS: A Review, Consortium of MS Centers, http://www.mscare.org, June 2007
  71. Cardini RG, Crippa AC, Cattaneo D (2000). Update on multiple sclerosis rehabilitation. J. Neurovirol. 6 Suppl 2: S179–85.
  72. ; Baclofen oral. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-17.
  73. Dantrolene oral. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-17.
  74. Diazepam. US National Library of Medicine (Medline) (2005-07-01). Retrieved on 2007-10-17.
  75. Tizanidine. US National Library of Medicine (Medline) (2005-07-01). Retrieved on 2007-10-17.
  76. Beard S, Hunn A, Wight J (2003). Treatments for spasticity and pain in multiple sclerosis: a systematic review. Health technology assessment (Winchester, England) 7 (40): iii, ix–x, 1–111.
  77. Paisley S, Beard S, Hunn A, Wight J (2002). Clinical effectiveness of oral treatments for spasticity in multiple sclerosis: a systematic review. Mult. Scler. 8 (4): 319–29.
  78. Becker WJ, Harris CJ, Long ML, Ablett DP, Klein GM, DeForge DA (1995). Long-term intrathecal baclofen therapy in patients with intractable spasticity. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 22 (3): 208–17.
  79. Koch M, Mostert J, Heersema D, De Keyser J (2007). Tremor in multiple sclerosis. J. Neurol. 254 (2): 133–45.
  80. Bozek CB, Kastrukoff LF, Wright JM, Perry TL, Larsen TA (1987). A controlled trial of isoniazid therapy for action tremor in multiple sclerosis. J. Neurol. 234 (1): 36–9.
  81. Duquette P, Pleines J, du Souich P (1985). Isoniazid for tremor in multiple sclerosis: a controlled trial. Neurology 35 (12): 1772–5.
  82. Hallett M, Lindsey JW, Adelstein BD, Riley PO (1985). Controlled trial of isoniazid therapy for severe postural cerebellar tremor in multiple sclerosis. Neurology 35 (9): 1374–7.
  83. Information from the USA National library of medicine on Isoniazid [12]
  84. Information from the USA National library of medicine on carbamazepine [13]
  85. Koller WC (1984). Pharmacologic trials in the treatment of cerebellar tremor. Arch. Neurol. 41 (3): 280–1.
  86. Sechi GP, Zuddas M, Piredda M, Agnetti V, Sau G, Piras ML, Tanca S, Rosati G (1989). Treatment of cerebellar tremors with carbamazepine: a controlled trial with long-term follow-up. Neurology 39 (8): 1113–5.
  87. Information from the USA National library of medicine on propanolol [14]
  88. Aisen ML, Holzer M, Rosen M, Dietz M, McDowell F (1991). Glutethimide treatment of disabling action tremor in patients with multiple sclerosis and traumatic brain injury. Arch. Neurol. 48 (5): 513–5.
  89. Mills RJ, Yap L, Young CA (2007). Treatment for ataxia in multiple sclerosis. Cochrane database of systematic reviews (Online) (1): CD005029.
  90. Aisen ML, Arnold A, Baiges I, Maxwell S, Rosen M (1993). The effect of mechanical damping loads on disabling action tremor. Neurology 43 (7): 1346–50.
  91. Bittar RG, Hyam J, Nandi D, Wang S, Liu X, Joint C, Bain PG, Gregory R, Stein J, Aziz TZ (2005). Thalamotomy versus thalamic stimulation for multiple sclerosis tremor. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 12 (6): 638–42.


Around Wikia's network

Random Wiki