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  Acute encephalitis

M. pneumoniae was strongly implicated as the probable etiologic agent in 1-10% children with acute encephalitis.


M. pneumoniae has been implicated as a cause of immunemediated neurologic syndromes, including ADEM, transversemyelitis, and Guillain-Barre´ syndrome

 

 Acute disseminated encephalomyelitis (ADEM)
Acute disseminated encephalomyelitis (ADEM) due to Mycoplasma pneumoniae infection in an adolescent.

 Acute disseminated encephalomyelitis developed after Mycoplasma pneumoniae infection complicating subclinical measles infection.


Novel myelin penta- and hexa-acetyl-galactosyl-ceramides: structural characterization and immunoreactivity in cerebrospinal fluid.

 

M. Koskiniemi, CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review, Clin Infect Dis 17 Suppl 1 (1993) S52-57.

S. Kusunoki, A. Chiba, S. Hitoshi, H. Takizawa, I. Kanazawa, Anti-Gal-C antibody in autoimmune neuropathies subsequent to mycoplasma infection, Muscle Nerve 18 (1995) 409-413.

A. Bitnun, E.L. Ford-Jones, M. Petric, D. MacGregor, H. Heurter, S. Nelson, G. Johnson, S. Richardson, Acute childhood encephalitis and Mycoplasma pneumoniae, Clin Infect Dis 32 (2001) 1674-1684.

M. Narita, H. Tanaka, T. Togashi, S. Abe, Cytokines involved in CNS manifestations caused by Mycoplasma pneumoniae, Pediatr Neurol 33 (2005) 105-109.

S. Tsiodras, I. Kelesidis, T. Kelesidis, E. Stamboulis, H. Giamarellou, Central nervous system manifestations of Mycoplasma pneumoniae infections, J Infect 51 (2005) 343-354.

F. Daxboeck, Mycoplasma pneumoniae central nervous system infections, Curr Opin Neurol 19 (2006) 374-378.

S. Tsiodras, T. Kelesidis, I. Kelesidis, K. Voumbourakis, H. Giamarellou, Mycoplasma pneumoniae-associated myelitis: a comprehensive review, Eur J Neurol 13 (2006) 112-124.

A. Harloff, S. Voigt, A. Hetzel, F.X. Glocker, T. Els, Severe axonal polyradiculoneuritis and brainstem encephalitis due to Mycoplasma pneumoniae infection, Eur J Neurol 9 (2002) 542-543.

F. Daxboeck, A. Blacky, R. Seidl, R. Krause, O. Assadian, Diagnosis, treatment, and prognosis of Mycoplasma pneumoniae childhood encephalitis: systematic review of 58 cases, J Child Neurol 19 (2004) 865-871.

K. Susuki, M. Odaka, M. Mori, K. Hirata, N. Yuki, Acute motor axonal neuropathy after Mycoplasma infection: Evidence of molecular mimicry, Neurology 62 (2004) 949-956.

R. Guleria, N. Nisar, T.C. Chawla, N.R. Biswas, Mycoplasma pneumoniae and central nervous system complications: a review, J Lab Clin Med 146 (2005) 55-63.

P.A. Mardh, B. Ursing, K. Lind, Persistent cerebellar symptoms after infection with Mycoplasma pneumoniae, Scand J Infect Dis 7 (1975) 157-160.

M.A. Hely, P.M. Williamson, T.R. Terenty, Neurological complications of Mycoplasma pneumoniae infection, Clin Exp Neurol 20 (1984) 153-160.

B. Goldschmidt, J. Menonna, J. Fortunato, P. Dowling, S. Cook, Mycoplasma antibody in Guillain-Barre syndrome and other neurological disorders, Ann Neurol 7 (1980) 108-112.

W.J. Shian, C.S. Chi, Acute transverse myelitis in children: clinical analysis of seven cases, Zhonghua Yi Xue Za Zhi (Taipei) 54 (1994) 57-61.

J.F. Albucher, D. Lauque, I. Geyer, J.D. Turc, F. Chollet, P. Carles, B. Guiraud-Chaumeil, [Transverse myelitis caused by Mycoplasma pneumoniae infection], Rev Neurol (Paris) 151 (1995) 350-353.

M. Abele-Horn, W. Franck, U. Busch, H. Nitschko, R. Roos, J. Heesemann, Transverse myelitis associated with Mycoplasma pneumoniae infection, Clin Infect Dis 26 (1998) 909-912.

Q. Hao, T. Saida, S. Kuroki, M. Nishimura, M. Nukina, H. Obayashi, K. Saida, Antibodies to gangliosides and galactocerebroside in patients with Guillain-Barre syndrome with preceding Campylobacter jejuni and other identified infections, J Neuroimmunol 81 (1998) 116-126.

B.C. Jacobs, P.H. Rothbarth, F.G. van der Meche, P. Herbrink, P.I. Schmitz, M.A. de Klerk, P.A. van Doorn, The spectrum of antecedent infections in Guillain-Barre syndrome: a case-control study, Neurology 51 (1998) 1110-1115.

R.A. Hughes, R.D. Hadden, N.A. Gregson, K.J. Smith, Pathogenesis of Guillain-Barre syndrome, J Neuroimmunol 100 (1999) 74-97.

S. Sotgiu, M. Pugliatti, G. Rosati, G.A. Deiana, G.P. Sechi, Neurological disorders associated with Mycoplasma pneumoniae infection, Eur J Neurol 10 (2003) 165-168.

C.W. Ang, A.P. Tio-Gillen, J. Groen, P. Herbrink, B.C. Jacobs, R. Van Koningsveld, A.D. Osterhaus, F.G. Van der Meche, P.A. van Doorn, Cross-reactive anti-galactocerebroside antibodies and Mycoplasma pneumoniae infections in Guillain-Barre syndrome, J Neuroimmunol 130 (2002) 179-183.

S. Kuwabara, Guillain-Barre syndrome: epidemiology, pathophysiology and management, Drugs 64 (2004) 597-610.

G.L. Nicolson, M.Y. Nasralla, J. Haier, J. Pomfret, High frequency of systemic mycoplasmal infections in Gulf War veterans and civilians with Amyotrophic Lateral Sclerosis (ALS), J Clin Neurosci 9 (2002) 525-529.

S. Sotgiu, M. Pugliatti, G. Rosati, G.A. Deiana, G.P. Sechi, Neurological disorders associated with Mycoplasma pneumoniae infection, Eur J Neurol 10 (2003) 165-168.


Guillain–Barré syndrome
Guillain–Barré syndrome (GBS) is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system.

The initial symptoms are typically changes in sensation or pain along with muscle weakness, beginning in the feet and hands. This often spreads to the arms and upper body.

The cause is unknown. The underlying mechanism involves an autoimmune disorder where the body's immune system mistakenly attacking the peripheral nerves and damaging their myelin insulation. Sometimes this immune dysfunction is triggered by an infection or less commonly surgery or vaccination.

There are a number of subtypes based on the areas of weakness, results of nerve conduction studies, and the presence of certain antibiodies. It is classified as an acute polyneuropathy.

Many people with Guillain–Barré syndrome have experienced the signs and symptoms of an infection in the 3–6 weeks prior to the onset of the neurological symptoms. This may consist of upper respiratory tract infection (rhinitis, sore throat) or diarrhea.

In the "Miller Fisher variant" subtype of Guillain–Barré syndrome (see below), weakness of the eye muscles (ophthalmoplegia) is more pronounced and may occur together with abnormalities in coordination (ataxia). The level of consciousness is normally unaffected in Guillain–Barré syndrome, but the Bickerstaff brainstem encephalitis subtype may feature drowsiness, sleepiness, or coma.

The autonomic or involuntary nervous system, which is involved in the control of body functions such as heart rate and blood pressure, is affected in two thirds of people with Guillain–Barré syndrome, but the impact is variable. Twenty percent may experience severe blood-pressure fluctuations and irregularities in the heart beat, sometimes to the point that the heart beat stops and requiring pacemaker-based treatment.

Two thirds of people with Guillain–Barré syndrome have experienced an infection before the onset of the condition. Most commonly these are episodes of gastroenteritis or a respiratory tract infection.

Mycoplasma pneumoniae have been associated with GBS.

The diagnosis of Guillain–Barré syndrome depends on findings such as rapid development of muscle paralysis, absent reflexes, absence of fever, and a likely cause.

Guillain–Barré syndrome and Mycoplasma Infectious Diseases (MID)
Mycoplasma antibody in Guillain-Barré syndrome and other neurological disorders.(1980)
http://www.ncbi.nlm.nih.gov/pubmed/7369715

Bilateral optic neuritis and Guillain-Barré syndrome following an acute Mycoplasma pneumoniae infection. (2004)
http://www.ncbi.nlm.nih.gov/pubmed/15311361

Meningitis associated with bilateral optic papillitis following Mycoplasma pneumoniae infection.(2012)
http://www.ncbi.nlm.nih.gov/pubmed/21732064

Acute central and peripheral demyelination associated with Mycoplasma pneumoniae.(2003)
http://www.ncbi.nlm.nih.gov/pubmed/14629909

Bell's palsy

C. Volter, J. Helms, B. Weissbrich, P. Rieckmann, M. Abele-Horn, Frequent detection of Mycoplasma pneumoniae in Bell's palsy, Eur Arch Otorhinolaryngol 261 (2004) 400-404.

Acute sensorineural hearing loss

T. Okada, I. Kato, I. Miho, S. Minami, H. Kinoshita, I. Akao, M. Kenmochi, S. Miyabe, I. Takeyama, Acute sensorineural hearing loss caused by Mycoplasma pneumoniae, Acta Otolaryngol Suppl 522 (1996) 22-25.

Chronic inflammatory demyelinating polyneuropathy(CIDP)
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated inflammatory disorder of the peripheral nervous system.

The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy (because it involves the nerve roots).

CIDP is closely related to Guillain-Barré syndrome and it is considered the chronic counterpart of that acute disease.

Chronic inflammatory demyelinating polyneuropathy is believed to be due to immune cells, which normally protect the body from foreign infection, incorrectly attacking the nerves in the body instead. As a result, the affected nerves fail to respond, or respond only weakly, to stimuli, causing numbing, tingling, pain, progressive muscle weakness, loss of deep tendon reflexes (areflexia), fatigue, and abnormal sensations.

Some patients may have sudden onset of back pain or neck pain radiating down the extremities, usually diagnosed as radicular pain.

Autonomic system dysfunction can occur; in such a case, the patient would complain of orthostatic dizziness, problems breathing, eye, bowel, bladder and cardiac problems.

The patient may also present with a single cranial nerve or peripheral nerve dysfunction.

CIDP is under-recognized and under-treated due to its heterogeneous presentation (both clinical and electrophysiological) and the limitations of clinical, serologic, and electrophysiologic diagnostic criteria.

Lack of awareness and treatment of CIDP is also due to limitations of clinical trials.

As in multiple sclerosis, another demyelinating condition, it is not possible to predict with certainty how CIDP is going to affect an individual in the future. The pattern of relapses and remissions varies greatly with each patient. A period of relapse can be very disturbing, but many patients make significant recoveries.

Chronic inflammatory demyelinating polyneuropathy and MID
Chronic inflammatory demyelinating polyneuropathy after Mycoplasma pneumoniae infection.(2007)
http://www.ncbi.nlm.nih.gov/pubmed/17594309

Atypical childhood chronic inflammatory demyelinating polyneuropathy. (2010)
http://www.ncbi.nlm.nih.gov/pubmed/20589891

Childhood chronic inflammatory demyelinating polyneuropathy: clinical course and long-term outcome. (2000)
http://www.ncbi.nlm.nih.gov/pubmed/10899445

   
       
       
       


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