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 after 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. Fifteen percent of individuals have multiple symptoms when they first seek medical attention.
The most common problems are an increase in frequency and urgency (incontinence) but difficulties to begin urination, hesitation, leaking, sensation of incomplete urination, and retention also appear. When retention occurs secondary urinary infections are common.
Treatment objectives are the alleviation of symptoms of urinary dysfunction, treatment of urinary infections, reduction of complicating factors and the 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 and some examples of the medications used are:alfuzosin for retention,trospium and flavoxate for urgency and incontinency, and desmopressin for nocturia. Non pharmacological treatments involve the use of pelvic floor muscle training, stimulation, biofeedback, pessaries, bladder retraining, and sometimes intermittent catheterization.
Bowel problems affect around 70% of the patients, with around 50% of the patients suffering from constipation and up to 30% from fecal incontinence. Cause of bowel impairments in MS patients is usually either a reduced gut motility or an impairment in neurological control of defecation. The former is commonly related to immobility or secondary effects from drugs used in the treatment of the disease. Pain or problems with defecation can be helped with a diet change which includes among other changes an increased fluid intake, oral laxatives or suppositories and enemas when habit changes and oral measures are not enough to control the problems.
Some of the most common deficits affect recent; memory, attention, processing speed, visual-spatial abilities and executive function. Symptoms related to cognition include emotional instability and fatigue including neurological fatigue. Commonly a form of cognitive disarray is experienced, where specific cognitive processes may remain unaffected, but cognitive processes as a whole are impaired. Cognitive deficits are independent of physical disability and can occur in the absence of neurological dysfunction. Severe impairment is a major predictor of a low quality of life, unemployment, caregiver distress, and difficulty in driving; limitations in a patient's social and work activities are also correlated with the extent of impairment.
Cognitive impairments occur in about 40 to 60 percent of patients with multiple sclerosis, with the lowest percentages usually from community-based studies and the highest ones from hospital-based. Impairments may present at the beginning of the disease. Probable multiple sclerosis sufferers, meaning after a first attack but before a secondary confirmatory one, have up to 50 percent of patients with impairment at onset.Dementia is rare and occurs in only five percent of patients.
Measures of tissue atrophy are well correlated with, and predict, cognitive dysfunction. Neuropsychological outcomes are highly correlated with linear measures of sub-cortical atrophy. Cognitive impairment is the result of not only tissue damage, but tissue repair and adaptive functional reorganization.Neuropsychological testing is important for determining the extent of cognitive deficits. Neuropsychological rehabilitation may help to reverse or decrease the cognitive deficits although studies on the issue have been of low quality.Acetylcholinesterase inhibitors are commonly used to treat Alzheimer's disease related dementia and so are thought to have potential in treating the cognitive deficits in multiple sclerosis. They have been found to be effective in preliminary clinical trials.
Emotional symptoms are also common and are thought to be both a 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. Brain imaging studies have tried to relate depression to lesions in certain regions of the brain have met with variable success. On balance the evidence seems to favour an association with neuropathology in the left anterior temporal/parietal regions.
Other feelings such as anger, anxiety, frustration, and hopelessness also appear frequently and suicide is a very real threat since it results in 15% of deaths in MS sufferers.
Fatigue is very common and disabling in MS with a close relationship to depressive symptomatology. When depression is reduced fatigue also tends to reduce and it is recommended that patients should be evaluated for depression before other therapeutic approaches are used. In a similar way other factors such as disturbed sleep, chronic pain, poor nutrition, or even some medications can all contribute to fatigue and medical professionals are encouraged to identify and modify them. There are also different medications used to treat fatigue; such as amantadine, or pemoline; as well as psychological interventions of energy conservation; but their effects are small and for these reasons fatigue is a difficult symptom to manage. Fatigue has also been related to specific brain areas in MS using magnetic resonance imaging.
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.
Different drugs as well as optic compensatory systems and prisms can be used to improve these symptoms. Surgery can also be used in some cases for this problem.
Animation created from an 1887 photographic study of locomotion of a MS male patient with walking difficulties by Muybridge
Restrictions in mobility (walking, transfers, bed mobility etc.) 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 (EDSS), requiring the use of a unilateral walking aid, and by 30 years the proportion increases to 83%. Within five years of onset the EDSS is six in 50% of those with the progressive form of MS.
A wide range of impairments may exist in MS sufferers 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.
Interventions may be aimed at the individual impairments that reduce mobility or at the level of disability. This second level intervention includes provision, education, and instruction in the use of equipment such as walking aids, wheelchairs, motorized scooters and car adaptations as well as instruction on compensatory strategies to accomplish an activity — for example undertaking safe transfers by pivoting in a flexed posture rather than standing up and stepping around.
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 MRIs at the time of presentation for optic neuritis is the strongest predictor in developing clinical diagnosis of MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis.
At five year follow-ups 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, 44% of patients with any demyelinating lesions on MRI at presentation will not have developed MS ten years later.
Individuals experience rapid onset of pain in one eye followed by blurry vision in part or all its visual field. Flashes of light (phosphenes) may also be present.Inflammation of the optic nerve causes loss of vision most usually by the swelling and destruction of the myelin sheath covering the optic nerve.
The blurred vision usually resolves within 10 weeks but individuals are often left with less vivid color vision, especially red, in the affected eye.
A systemic intravenous treatment with corticosteroids may quicken the healing of the optic nerve, prevent complete loss of vision and delay the onset of other symptoms.
Pain is a common symptom in MS. A recent study systematically pooling results from 28 studies (7101 patients) estimates that pain affects 63% of people with MS. These 28 studies described pain in a large range of different people with MS. The authors found no evidence that pain was more common in people with progressive types of MS, in females compared to males, in people with different levels of disability, or in people who had had MS for different periods of time.
Pain can be severe and debilitating, and can have a profound effect on the quality of life and mental health of the sufferer. Certain types of pain are thought to sometimes appear 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. The most prevalent types of pain are thought to be headaches (43%), dysesthetic limb pain (26%), back pain (20%), painful spasms (15%), painful Lhermitte's phenomenon (16%) and Trigeminal Neuralgia (3%). These authors did not however find enough data to quantify the prevalence of painful optic neuritis.
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, affecting 2-4% of MS patients. The episodes of pain occur paroxysmally (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 is successfully treated with anticonvulsants such as carbamazepine, or phenytoin although others such as gabapentin can be used. When drugs are not effective, surgery may be recommended. Glycerol rhizotomy (surgical injection of glycerol into a nerve) has been studied although the beneficial effects and risks in MS patients of the procedures that relieve pressure on the nerve are still under discussion.
Lhermitte's sign is an electrical sensation that runs down the back and into the limbs and is produced by bending the neck forwards. The sign suggests a lesion of the dorsal columns of the cervical cord or of the caudal medulla, correlating significantly with cervical MRI abnormalities. Between 25 and 40% of MS patients report having Lhermitte's sign during the course of their illness. It is not always experienced as painful, but about 16% of people with MS will experience painful Lhermitte's sign.
Dysesthesias are disagreeable sensations produced by ordinary stimuli. The abnormal sensations are caused by lesions of the peripheral or central sensory pathways, and are described as painful feelings such as burning, wetness, itching, electric shock or pins and needles. Both Lhermitte's sign and painful dysesthesias usually respond well to treatment with carbamazepine, clonazepam or amitriptyline. A related symptom is a pleasant, yet unsettling sensation which has no normal explanation (such as sensation of gentle warmth arising from touch by clothing)
Sexual dysfunction (SD) is one of many symptoms affecting persons with a diagnosis of MS. SD in men encompasses both erectile and ejaculatory disorder. The prevalence of SD in men with MS ranges from 75 to 91%. Erectile dysfunction appears to be the most common form of SD documented in MS. SD may be due to alteration of the ejaculatory reflex which can be affected by neurological conditions such as MS. Sexual dysfunction is also prevalent in female MS patients, typically lack of orgasm, probably related to disordered genital sensation.
Photographic study of locomotion of a MS female patient with walking difficulties and spasticity created in 1887 by Muybridge
Speech problems include slurred speech, low tone of voice (dysphonia), decreased talking speed, and problems with articulation of sounds (dysarthria). A related problem, since it involves similar anatomical structures, is swallowing difficulties (dysphagia).
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 nerve cords 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.
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 and present in 25 to 60% of patients. They can be very disabling and embarrassing, and are difficult to manage. The origin of tremor in MS is difficult to identify but it can be due to a mixture of different factors such as damage to the cerebellar connections, weakness, spasticity, etc.
Many medications have been proposed to treat tremor; however their efficacy is very limited. Medications that have been reported to provide some relief are isoniazid,carbamazepine,propranolol and gluthetimide but published evidence of effectiveness is limited.Physical therapy is not indicated as a treatment for tremor or ataxia although the use of 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. Daily use objects are also adapted so they are easier to grab and use.
If all these measures fail patients are candidates for thalamussurgery. 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 though the higher incidence of persistent neurological deficits in patients receiving lesional surgery supports the use of deep brain stimulation as the preferred surgical strategy.
^Kurtzke JF (1983). "Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS)". Neurology33 (11): 1444–52. doi:10.1212/WNL.33.11.1444. PMID6685237.
^Navarro S, Mondéjar-Marín B, Pedrosa-Guerrero A, Pérez-Molina I, Garrido-Robres J, Alvarez-Tejerina A (2005). "[Aphasia and parietal syndrome as the presenting symptoms of a demyelinating disease with pseudotumoral lesions]". Rev Neurol41 (10): 601–3. PMID16288423.
^Paty D, Studney D, Redekop K, Lublin F (1994). "MS COSTAR: a computerized patient record adapted for clinical research purposes". Annals of Neurology. 36 Suppl: S134–5. doi:10.1002/ana.410360732. PMID8017875.
^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. doi:10.1007/s004150050508. PMID10631634.
^Burguera-Hernández JA (2000). "[Urinary alterations in multiple sclerosis]". Revista de neurologia (in Spanish) 30 (10): 989–92. PMID10919202.
^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. doi:10.1111/j.1600-0404.2005.00431.x. PMID15932348.
^Information from the USA National library of medicine on desmopressin 
^ abBenedict RH, Carone DA, Bakshi R (July 2004). "Correlating brain atrophy with cognitive dysfunction, mood disturbances, and personality disorder in multiple sclerosis". J Neuroimaging14 (3 Suppl): 36S–45S. doi:10.1177/1051228404266267. PMID15228758.
^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 Rehabil83 (8): 1123–9. doi:10.1053/apmr.2002.33730. PMID12161835.
^Rao S, Leo G, Bernardin L, Unverzagt F (1991). "Cognitive dysfunction in multiple sclerosis. I. Frequency, patterns, and prediction". Neurology41 (5): 685–91. doi:10.1212/wnl.41.5.685. PMID2027484.
^ abcThe Royal College of Physicians (2004). Multiple Sclerosis. National clinical guideline for diagnosis and management in primary and secondary care. Salisbury, Wiltshire: Sarum ColourView Group. ISBN1-86016-182-0.Free full text (2004-08-13). Retrieved on 2007-10-01.
^Pucci E, Branãs P, D'Amico R, Giuliani G, Solari A, Taus C (2007). Pucci, Eugenio, ed. "Amantadine for fatigue in multiple sclerosis". Cochrane database of systematic reviews (Online) (1): CD002818. doi:10.1002/14651858.CD002818.pub2. PMID17253480.
^Amantadine. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-07.
^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". Neurology42 (8): 1468–71. doi:10.1212/wnl.42.8.1468. PMID1641137.
^Pemoline. US National Library of Medicine (Medline) (2006-01-01). Retrieved on 2007-10-07.
^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. doi:10.1191/1352458505ms1198oa. PMID16193899.
^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 Therapy61 (1): 62–9. doi:10.5014/ajot.61.1.62. PMID17302106.
^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.15 (3): 337–44. doi:10.1177/1352458508098373. PMID18987107.
^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". Annals of Neurology36 (2): 129–41. doi:10.1002/ana.410360204. PMID8053648.
^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. doi:10.1007/PL00007728. PMID9007739.
^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. doi:10.1038/sj.eye.6700167. PMID12439689.
^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. doi:10.1016/S0002-9394(02)01629-X. PMID12429265.
^Weinshenker BG, Bass B, Rice GP, et al. (1989). "The natural history of multiple sclerosis: a geographically based study. I. Clinical course and disability". Brain112 (1): 133–46. doi:10.1093/brain/112.1.133. PMID2917275.
^ abcdeFoley P, Vesterinen H, Laird B et al (2013). "Prevalence and natural history of pain in adults with multiple sclerosis: Systematic review and meta-analysis". Pain154 (5): 632–42. doi:10.1016/j.pain.2012.12.002. PMID23318126.
^Archibald CJ, McGrath PJ, Ritvo PG, et al. (1994). "Pain prevalence, severity and impact in a clinic sample of multiple sclerosis patients". Pain58 (1): 89–93. doi:10.1016/0304-3959(94)90188-0.
^Kerns RD, Kassirer M, Otis J (2002). "Pain in multiple sclerosis: a biopsychosocial perspective". Journal of rehabilitation research and development39 (2): 225–32. PMID12051466.
^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. doi:10.1159/000008192. PMID10894995.
^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 neurologiques21 (2): 137–40. PMID8087740.
^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 neurosurgery19 (6): 463–8. doi:10.1080/02688690500495067. PMID16574557.
^Eldridge PR, Sinha AK, Javadpour M, Littlechild P, Varma TR (2003). "Microvascular decompression for trigeminal neuralgia in patients with multiple sclerosis". Stereotactic and functional neurosurgery81 (1–4): 57–64. doi:10.1159/000075105. PMID14742965.
^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. doi:10.3109/00207459509004888. PMID7628912.
^Baclofen oral. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-17.
^Dantrolene oral. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-17.
^Diazepam. US National Library of Medicine (Medline) (2005-07-01). Retrieved on 2007-10-17.
^Tizanidine. US National Library of Medicine (Medline) (2005-07-01). Retrieved on 2007-10-17.
^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. PMID14636486.
^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. doi:10.1191/1352458502ms795rr. PMID12166503.
^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 neurologiques22 (3): 208–17. PMID8529173.
^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. doi:10.1007/BF00314007. PMID3546605.
^Hallett M, Lindsey JW, Adelstein BD, Riley PO (1985). "Controlled trial of isoniazid therapy for severe postural cerebellar tremor in multiple sclerosis". Neurology35 (9): 1374–7. doi:10.1212/wnl.35.9.1374. PMID3895037.
^Information from the USA National library of medicine on Isoniazid 
^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". Neurology39 (8): 1113–5. doi:10.1212/wnl.39.8.1113. PMID2668787.
^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. doi:10.1001/archneur.1991.00530170077023. PMID2021365.