DT
вот и
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2017 May 22
DT
какой то из них сирингомиелия
DT
а какойто энцефаломиелит
SS
bunda sirengomieliya
SS
capsulasi bn
SS
энсефаломиелит белгисини топомадим ториси
DT
Курсатганиз энцефаломиелит
DT
Бутда киари бор
DT
Сирингомиелия бн
DT
A 58-year-old retired female office clerk presented to the emergency services
with dysphagia and leg weakness. Seven years previously, she had developed a
cervical transverse myelitis which had resolved and then recurred 2 years later
following which she was diagnosed with multiple sclerosis. Over the next 4 years
she had several relapses that all presented with cord symptoms although brain
MRI also showed demyelination. She had received treatment with interferon.
Three weeks prior to presentation, she was seen by her general practitioner
with bilateral arm weakness and left leg weakness that had come on gradually
over the previous 3 days. This was accompanied by tingling in the arms and
legs that was possibly old. The general practitioner gave a 5-day course of
prednisolone with initial improvement in her symptoms. One week before
presentation, she developed dysphagia, nasal regurgitation, nasal voice and
increasing limb weakness. There were no eye symptoms. Three days before,
her face and upper limbs began to swell and the limb weakness worsened.
She was not on any medication. There was no family history or past medical
history of note, she was an ex-smoker, and took minimal alcohol.
On examination, the arms and neck were oedematous and tender and the
skin was flushed. There was mild lower limb oedema. General and breast
examination was unremarkable. Her voice was weak with a poor cough. There
was a left Horner’s syndrome, weakness of eye closures and decreased palatal
elevation. Swallow was impaired. Power was reduced proximally (severely in
the lower limbs and moderately in the lower limbs) and to a lesser extent distally.
Reflexes were absent in the upper limbs and ankles but present with reinforcement
at the knees. Both plantars were upgoing. Vibration sense was
reduced in both upper and lower limbs.
with dysphagia and leg weakness. Seven years previously, she had developed a
cervical transverse myelitis which had resolved and then recurred 2 years later
following which she was diagnosed with multiple sclerosis. Over the next 4 years
she had several relapses that all presented with cord symptoms although brain
MRI also showed demyelination. She had received treatment with interferon.
Three weeks prior to presentation, she was seen by her general practitioner
with bilateral arm weakness and left leg weakness that had come on gradually
over the previous 3 days. This was accompanied by tingling in the arms and
legs that was possibly old. The general practitioner gave a 5-day course of
prednisolone with initial improvement in her symptoms. One week before
presentation, she developed dysphagia, nasal regurgitation, nasal voice and
increasing limb weakness. There were no eye symptoms. Three days before,
her face and upper limbs began to swell and the limb weakness worsened.
She was not on any medication. There was no family history or past medical
history of note, she was an ex-smoker, and took minimal alcohol.
On examination, the arms and neck were oedematous and tender and the
skin was flushed. There was mild lower limb oedema. General and breast
examination was unremarkable. Her voice was weak with a poor cough. There
was a left Horner’s syndrome, weakness of eye closures and decreased palatal
elevation. Swallow was impaired. Power was reduced proximally (severely in
the lower limbs and moderately in the lower limbs) and to a lesser extent distally.
Reflexes were absent in the upper limbs and ankles but present with reinforcement
at the knees. Both plantars were upgoing. Vibration sense was
reduced in both upper and lower limbs.
SS
Курсатганиз энцефаломиелит
я пас😂
DT
добрый вечер коллеги
DT
есть ответ на кейс?
DT
ответ дерматомиозит
DT
A 38-year-old man presented to the emergency department complaining of
unsteadiness and dizziness and a fall in which he suffered a minor head injury
with no loss of consciousness. No abnormality was found on examination and
a skull X-ray was unremarkable. He re-presented 1 week later with a further
minor head injury without loss of consciousness and reported ongoing
unsteadiness and dizziness, difficulty walking and blurred vision, and was
admitted to hospital. He worked as a chemistry laboratory technician and
occupied an office containing discarded experimental equipment. Past medical
history included investigation for diarrhoea and possible malabsorbtion
(for which he had been put on a gluten-free diet). Examination revealed symmetrical
incoordination consistent with cerebellar dysfunction and bilateral
nystagmus on lateral gaze.
The following investigations were normal:
● CT brain scan,
● FBC, ESR, U&E, TFT, LFT,
● B12, folate,
● CXR, and MRI brain.
● MCV was 100fL.
On examination one week after admission, he was noted to have a strange
affect and was talkative but not unwell. He complained of poor memory,
blurred vision, fatigue, and inability to concentrate. His hearing was reduced
on the right more than the left, the limbs were normal but his coordination
was still impaired.
unsteadiness and dizziness and a fall in which he suffered a minor head injury
with no loss of consciousness. No abnormality was found on examination and
a skull X-ray was unremarkable. He re-presented 1 week later with a further
minor head injury without loss of consciousness and reported ongoing
unsteadiness and dizziness, difficulty walking and blurred vision, and was
admitted to hospital. He worked as a chemistry laboratory technician and
occupied an office containing discarded experimental equipment. Past medical
history included investigation for diarrhoea and possible malabsorbtion
(for which he had been put on a gluten-free diet). Examination revealed symmetrical
incoordination consistent with cerebellar dysfunction and bilateral
nystagmus on lateral gaze.
The following investigations were normal:
● CT brain scan,
● FBC, ESR, U&E, TFT, LFT,
● B12, folate,
● CXR, and MRI brain.
● MCV was 100fL.
On examination one week after admission, he was noted to have a strange
affect and was talkative but not unwell. He complained of poor memory,
blurred vision, fatigue, and inability to concentrate. His hearing was reduced
on the right more than the left, the limbs were normal but his coordination
was still impaired.
ℳ
Отравление ртутью у него.
DT
DT
A 30-year-old Polish man was admitted to hospital with confusion and aggressive
behaviour. The history was obtained from friends.He had been unwell for
the previous 5 days with fever and headache and over the 2 days prior to
admission had suffered several episodes of vomiting and complained of a stiff
neck. He had been working in the UK as a labourer for the preceding year and
had not left the UK during that period. His wife had remained in Poland.
None of his friends or workmates had been unwell. He had had one or two
brief sexual relationships since his arrival in the UK. There was no past medical
history.
On examination, he was uncooperative, agitated and aggressive with
confused speech, according to his friends. The temperature was elevated
at 37.9°C but general systems examination was otherwise unremarkable.
There was neck stiffness and mild photophobia but no focal neurological
abnormality.
Investigations showed:
● Hb 15g/dL,WCC 8.2 × 109/L, plt 211 × 109/L
● Na 133mmol/L, K 3.2mm/L, urea 6.0mmol/L and Cr 130μmol/L.
● CRP 22mg/L
● CXR: normal
● CT brain: normal
● LP: CSF opening pressure 32cm H2O, colourless appearance,
WCC 488/mm3 (64 polymorphs, 424 lymphocytes, 46 red blood
cells), protein 2.04g/L, glucose 1.1mmol/L (5.5mmol/L blood),
no organisms seen on gram stain, AFB stain negative, Indian ink stain
negative.
Initial treatment was with ceftriaxone and aciclovir. The day after admission
he was more settled but developed a complete left ptosis with a fixed and
dilated pupil and inability to adduct, elevate or abduct the left eye. His condition
was otherwise unchanged.
Further investigations showed:
● CT brain with contrast: normal.
● Repeat LP: 770 white cells/mm3 (70 polymorphs, 700 lymphocytes and
30 red blood cells).
behaviour. The history was obtained from friends.He had been unwell for
the previous 5 days with fever and headache and over the 2 days prior to
admission had suffered several episodes of vomiting and complained of a stiff
neck. He had been working in the UK as a labourer for the preceding year and
had not left the UK during that period. His wife had remained in Poland.
None of his friends or workmates had been unwell. He had had one or two
brief sexual relationships since his arrival in the UK. There was no past medical
history.
On examination, he was uncooperative, agitated and aggressive with
confused speech, according to his friends. The temperature was elevated
at 37.9°C but general systems examination was otherwise unremarkable.
There was neck stiffness and mild photophobia but no focal neurological
abnormality.
Investigations showed:
● Hb 15g/dL,WCC 8.2 × 109/L, plt 211 × 109/L
● Na 133mmol/L, K 3.2mm/L, urea 6.0mmol/L and Cr 130μmol/L.
● CRP 22mg/L
● CXR: normal
● CT brain: normal
● LP: CSF opening pressure 32cm H2O, colourless appearance,
WCC 488/mm3 (64 polymorphs, 424 lymphocytes, 46 red blood
cells), protein 2.04g/L, glucose 1.1mmol/L (5.5mmol/L blood),
no organisms seen on gram stain, AFB stain negative, Indian ink stain
negative.
Initial treatment was with ceftriaxone and aciclovir. The day after admission
he was more settled but developed a complete left ptosis with a fixed and
dilated pupil and inability to adduct, elevate or abduct the left eye. His condition
was otherwise unchanged.
Further investigations showed:
● CT brain with contrast: normal.
● Repeat LP: 770 white cells/mm3 (70 polymorphs, 700 lymphocytes and
30 red blood cells).
E
Herpetic encephalitis with left third palsy