This guideline covers diagnosing, assessing and managing cerebral palsy in children and young people from birth up to their 25th birthday. It aims to make sure they get the care and treatment they need for the developmental and clinical comorbidities associated with cerebral palsy, so that they can be as active and independent as possible

Recommendations This guideline includes recommendations on: 

• ​causes and recognition of cerebral palsy
• multidisciplinary care and information and support
• managing feeding and drooling problems
• support with speech, language and communication
• assessing and managing pain, discomfort, distress and sleep disturbances
• information on other comorbidities, including mental health problems
• transition to adults' services
  

Picture courtesy: Inspirational Bailey Matthews was roared over the finishing line by crowds close to tears as he cast aside his specially-adapted walking frame to finish the last 20 metres of the race unaided at the Castle Howard Triathlon in North Yorkshire 2015

In a study have been published in the journal Neurology researchers from Charité - Universitätsmedizin Berlin and the German Center for Neurodegenerative Diseases (DZNE) using a new treatment regimen have recorded significant progress in patients with Anti-NMDA receptor encephalitis.  In addition to standard treatment, patients received bortezomib, a drug known as proteasome inhibitor that has proven successful in treating patients with plasmacytoma a haematological malignancy. Proteasomes play an important role in the degradation of proteins that regulate the cell cycle, thereby regulating cell growth. Given their high rates of protein synthesis, antibody-producing plasma cells display particularly high levels of metabolic activity. This renders them as sensitive to the effects of the drug as cancer cells, and results in their death.

Five severely affected patients with anti-NMDAR encephalitis with delayed treatment response or resistance to standard immunosuppressive and B-cell-depleting drugs (corticosteroids, IV immunoglobulins, plasma exchange, immunoadsorption, rituximab, cyclophosphamide) who required medical treatment and artificial ventilation on intensive care units were treated with 1–6 cycles of 1.3 mg/m2 bortezomib

Bortezomib treatment showed clinical improvement or disease remission, which was accompanied by a partial NMDAR antibody titer decline in 4 of 5 patients. With respect to disease severity, addition of bortezomib to the multimodal immunosuppressive treatment regimen was associated with an acceptable safety profile.

"'Bortezomib is capable of treating the causes of the disease by eliminating plasma cells. This makes it a valuable new treatment option in cases of anti-NMDA receptor encephalitis that have so far proven resistant to treatment," explains Franziska Scheibe, the study's first author. The results need to be confirmed by randomized trials as is the case with all the other treatment currently used in anti NMDA receptor encephalitis patients.

Structure of the Zika Virus

A systematic review of the evidence confirms that infection with mosquito-borne Zika virus is a cause of Guillain-Barre Syndrome (GBS), in addition to microcephaly and other congenital brain abnormalities, according to a study published in PLOS Medicine by Nicola Low of the University of Bern, Switzerland, and colleagues in the World Health Organization (WHO) Zika Causality Working Group. 

In March 2016, WHO stated that there was a strong scientific consensus that Zika virus is a cause of GBS, microcephaly, and other neurological disorders. However, decisions about causality must be assessed systematically to guide public health actions. In the new work, the WHO group defined specific questions about the relationship between Zika virus and clinical outcomes, setting a framework of ten dimensions to define causality. They then reviewed existing literature for studies that addressed the outcomes - either GBS or congenital brain abnormalities - and convened a panel of experts to assess the review findings. 

Based on 72 studies published up to May 30, 2016, that included data on Zika and congenital brain abnormalities, the team concluded that at least eight of the ten criteria for causality were met. Based on 36 studies published in the same time frame with data on Zika and GBS, the researchers concluded that at least seven of the ten criteria for causality were met. In addition, papers published after the initial literature review - between May 30 and July 29, 2016 - strengthened the initial findings that Zika virus is causative of brain abnormalities and GBS. 

Rapid and systematic reviews with frequent updating and open disseminating are now needed, both for appraisal of the evidence about Zika virus infection and for the next public health threats that will emerge

However, there are remaining questions about the link that will need to be addressed with continuing studies. The review was funded by the World Health Organization (http://www.who.int/en/, contract numbers 2016/611294-0 and 2016/630126-0 awarded to NL) and the Swiss National Science Foundation (www.snf.ch, SNSF special action fund and project grant 320030_170069 awarded to NL). The WHO Zika Causality Working Group was involved in interpretation of the data and the decision to publish. 

​Article: Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain-Barré Syndrome: Systematic Review, Krauer F, Riesen M, Reveiz L, Oladapo OT, Martínez-Vega R, Porgo TV, et al., PLOS Medicine, doi: 10.1371/journal.pmed.1002203, published 3 January 2016...

SPINRAZA (nusinersen) is an antisense oligonucleotide (ASO) that is designed to treat SMA caused by mutations in the chromosome 5q that leads to SMN protein deficiency. SPINRAZA (nusinersen) alters the splicing of SMN2 pre-mRNA in order to increase production of full-length SMN protein. ASOs are short synthetic strings of nucleotides designed to selectively bind to target RNA and regulate gene expression. Through use of this technology, SPINRAZA (nusinersen) has the potential to increase the amount of full-length SMN protein in patients with SMA. 

SPINRAZA (nusinersen) is administered via intrathecal injection, which delivers therapies directly to the cerebrospinal fluid (CSF) around the spinal cord, where motor neurons degenerate in patients with SMA due to insufficient levels of SMN protein.

The most common adverse reactions reported for SPINRAZA (nusinersen) were upper respiratory infection, lower respiratory infection and constipation. Serious adverse reactions of atelectasis were more frequent in SPINRAZA (nusinersen)-treated patients. Coagulation abnormalities and thrombocytopenia, including acute severe thrombocytopenia, have been observed after administration of some antisense oligonucleotides. 

Renal toxicity, including potentially fatal glomerulonephritis, has been observed after administration of some antisense oligonucleotides.