Sol chronic antiparkinsonian drugs levodopa or

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-detoxification: dilution with infusion therapy (Saline, Glucose, or Hemodilution with prot. Sol.) -Chronic: Antiparkinsonian Drugs (Levodopa or central anticholinesterase drugs) -Antiepileptic drugs: (Clonazepam or Carbamazepine) -Cholinesterase inhibitors: Neostigmine 28. Tick borne encephalitis: *Epidemiology: -Seen in spring and autumn time (when ticks are active) -spatial distribution: more seen in patients coming from forrest/maountain areas than in urban citizens -all ages possible, equal male to female ratio -Vector of transmission is the Tick with a bite, and very rare, the consumption of inected meat -incubation period is 7d – 1 month -caused by a Neurovirus *Clinical presentation: -high temperature -headache, fatigue -non-specific somatic symptoms (nausea, diarrhea, jaundice) -neurological signs develop after several days *Forms: *aborting form: only short stage of non-specific sign *meningeal form: acute viral meningitis, headache, vomiting, meningeal syndrome, benign course *bulbo-pontine form: more Severe -involvement of the brainstem, affection of the upper cervical segments -affection of cranial nerves: bilateral paralysis of n. Facialis and masticatory muscles -bulbar syndrome -paralysis of head motions and upper girdle muscles -after recovery patient may suffer from motor deficit *encephalitic form: most severe (fatal outcome) -affection of cortex, midbrain and brainstem -coma -generalized epileptic seizures -hemiparesis -autonomic disorders -bulbar syndrome *meningeal encephalitis: -neural affection -meningeal irritation (meningeal syndrome) -headache, vomiting -combination of meningeal and encephalitic form
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*Diagnosis: -Confirm Tick bite (big round hyperemic focus with pale center – bullseye) -immunological measurement of antiviral antibody titre in blood *Treatment: -non-specific antiviral therapy: I.V. infusion of human immunoglobulins, gamma interferones, interferone inducers, amantadine -aggressive detoxification therapy: glucose infusions, hemodilution -antiedeatous therapy: diuretics (Prognosis is determined by early onset of treatment) 29. Cerebral Arachnoiditis: *Causes: -head injuries or their long term consequences -neuroinfections -after neurosurgical interventions -purulent ear diseases *pathogenesis and epidemiology -affection of the arachnoid matter -also calles leptomeningitis (inflammation of the arachnoid and pia mater) -formation of postinflamatory adhesion scars (chronic) -persists till the end of patients life -causes problems with CSF circulation and absorption -leads to compression of cranial nerves *Classification: (according to anatomical location of lesions in chronic stage) -optochiasmatic arachnoiditis -pontocerebellar angle (borderline btw brainstem and cerebellum) -convexical: above cortex *clinical presentation: *acute stage -subfebrile temperature -headache of moderate intensity -nausea and vomiting (due to brain edema) -meningeal signs (sometimes) *Chronic stage -signs determined by anatomical location of lesion -chronic flucturating headache which increases with increased ICP (together with nausea and vomit.) -progressive visual loss, even blindness -mild cognitive decline, problems with concentration, studying
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  • Winter '18
  • Jane doe

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