Cauda equina syndrome

a 82-year-old female, a case of Surface serous papillary carcinoma s/p chemotherapy, complained of lower back soreness radiating to the lower limbs, hypoesthesia at peri-anal area, sphincter disturbance with urinary retention and difficulty in defecation for 4-5 months.

姓名：吳oo 女士 生日： 0140108
病歷號：3228124 照會單號：T0089251030
檢查項目 .....檢查日期：2008-06-02
MRI With/Without Contrast--Spine
報告內容 ...
Hx: SSPC, s/p LSC with biopsy, s/p PT *6. recurrence, s/p PT *6, recurrence, s/p Lipodox and Carboplatin *6

MRI of L spine without/with contrast enhancement shows
1. multiple enhancing enhancing nodules noted along the pial surface of visible spinal cord, abnormal enhancement along the cauda equina and nodular enhancement of nerve roots in the sacral canal. CSF tumor seeding is considered.
2. suspicious mild edematous change of the spinal cord aroud the nodules
3. lumbar spondylosis with marginal spur formation and bulging disc at L1 to L5 level, accompanied by mild hypertrophy of facet joints and ligamentum flavum. They result in mild narrowing of thecal sac.
4. normal alignment of L spine, no focal bony destruction is found.
5. the paraspinal soft tissue is unremarkable.



Impression
CSF tumor seeding, along the pial surface of the spinal cord and cauda equina. mild lumbar spondylosis

new stroke in old CVA patient?

a dominent-personality patient with old stroke with mild right hemiparesis, complained of right limb heavy sensation, acute onset for 1 week.
He asked for brain MRI. The NE showed mild right hemiparesis with spasticity. Hepatitis due to Plavix? was told. Brain MRI was arranged to exclude new stroke in this patient. 羅oo(M,63_6) 1698992
Brain MRI (2008/05/13)

T-myelopathy with lower limb paresthesia

T-myelopathy with lower limb paresthesia

姓名:葉OO 病歷號:5298068

48 male, actue onset of LE numbness, buttock tightness up to the umbilicus on 2008/4/2-3

LE weakness, unsteady gait with floating sensation, lower limbs weakness improved by itself

Spine MRI showed a mid-T HIVD with cord compression.

CSF study at other hospital was normal.

SSEP was arranged.

dizziness, unsteady gait for 3 days

a 80y/o man, HTN, CAD s/p CABG,
c/o: dizziness, vertigo, nausea, unsteady gait to either direction, unable to walk for 3 days
NE: mildly drowsy, limbs ataxia bilaterally UE & LE, truncal ataxia
MP 5/5
no abducens palsy
Head CT: heterogenous hyperintensities with perifocal hypodensity in the right cerebellum, mild hydrocephalus
Brain MRI:
姓名：許 先生 生日： 0160729
病歷號：2708662 照會單號：2655160
檢查項目 .....檢查日期：2008-04-16
MRI-HEAD

MRI of head without/with contrast enhancement shows
1. a large irregular shaped acute hematoma in right superior cerebelum, showing hypointensity with minimal patchy hyperintensities on T1WI, mild hypointensity on T2WI with focal fluid-fluid layering suggestive of noncoagulant blood. The hematoma extends along the gyrus . There is no obvious abnormal enhancement after contrast injection. Hemorrhagic infarction in right SCA territory is most favored.
2. DWI shows minimal bright up along the margin of hematoma.
3. the brainstem and 4th ventricle are compressed with dilatation of both lateral and the 3rd ventricles. The degree of hydrocephalus is similar as compared with CT study
4. multiple nonspecific hyperintense patches on T2WI at bil. PVWM, leukoaraiosis is considered.
5. contrast-enhanced MRA of cervicocranial vessels shows moderate stenosis of left proximal ICA
6. the cranial vault and skull base appear normal

Impression
Hemorrhagic infarction in right SCA territory, with mass effect and mild hydrocephalus Mild nonspecific white matter change.

Q: indication of surgical decompression of cerebellar lesion with risk of brainstem compression?
Surgical Care

* Indications for surgery are controversial.
* Ventriculostomy is indicated in patients with hemorrhage and hydrocephalus.
* Suboccipital craniotomy with clot evacuation is indicated in patients with altered level of consciousness and a large clot (>30 mm but no greater than 40 mm).
* Patients with a large central clot and absent brainstem reflexes have a poor prognosis. In these cases, some advocate supportive therapy only.
* Patients may appear to be in stable condition but can worsen suddenly. St Louis et al list clinical and CT findings that may identify patients who are at risk for deterioration.
*
o Admission systolic blood pressure greater than 200 mm Hg
o Pinpoint pupils and abnormal corneal and oculocephalic reflexes
o Hemorrhage extending into the cerebellar vermis
o Hematoma diameter greater than 30 mm
o Brainstem distortion
o Intraventricular hemorrhage
o Upward herniation
o Acute hydrocephalus
* CT-guided stereotactic fibrinolysis of the hematoma has been reported in small numbers of carefully selected patients.
* Endoscopic hematoma evacuation has also been reported to have been effective in a small number of patients.

Consultations

* Consult neurosurgery for all patients, even those who are candidates for conservative management. Sudden deterioration may require neurosurgical intervention.



Further Inpatient Care

* Ideally, admit patients to the care of critical care physicians with expertise in managing intracranial hemorrhages.
* Careful monitoring for level of consciousness, vital signs, and ICP is needed for some patients.
* The risk of sudden deterioration is high and mandates the attention that is available in an intensive care unit.
* If immediate surgical intervention is deferred, a deteriorating clinical course may necessitate surgery at a later time.
*
o Posterior fossa craniotomy and evacuation of the hemorrhage may be necessary for patients with worsening clinical condition.
o If surgical therapy is prompt, some comatose patients still may have a good clinical outcome.
* Physical and occupational therapy may be useful in patients who are in stable condition.

1: Clin Neurol Neurosurg. 1998 Jun;100(2):99-103.
Related Articles, Links
Click here to read
Indication to surgical management of cerebellar hemorrhage.

Pollak L, Rabey JM, Gur R, Schiffer J.

Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel.

Few reports have compared patients operated for cerebellar infarcts with those operated for cerebellar hemorrhage. Considering our previous paper about patients with massive cerebellar infarcts, we report on our surgical experience with five patients with cerebellar hemorrhage. The indication for operation was decreased consciousness with signs of brainstem compression. In all patients hydrocephalus was absent or mild, as opposed to patients with cerebellar infarcts. Suboccipital craniotomy with hematoma evacuation was therefore the surgical procedure of choice. The outcome was worse than in patients with cerebellar infarcts. We conclude that depressed mental state in cerebellar hemorrhage is mainly due to pressure of the cerebellum on the activating reticular system of the brainstem. The surgical approach to patients with bleeding in the cerebellum differ somewhat from that of patients with cerebellar infarcts in timing and kind of first choice procedure.

Lancet Neurol. 2005 Oct;4(10):662-72.Click here to read Links
Treatment of intracerebral haemorrhage.
Mayer SA, Rincon F.

Neurological Intensive Care Unit, Division of Stroke and Critical Care, Department of Neurology Columbia University, New York, NY 10032, USA. sam14@columbia.edu

Apart from management in a specialised stroke or neurological intensive care unit, until very recently no specific therapies improved outcome after intracerebral haemorrhage (ICH). In a recent phase II trial, recombinant activated factor VII (eptacog alfa) reduced haematoma expansion, mortality, and disability when given within 4 h of ICH onset; a phase III trial (the FAST trial) is now in progress. Ventilatory support, blood-pressure reduction, intracranial-pressure monitoring, osmotherapy, fever control, seizure prophylaxis, and nutritional supplementation are the cornerstones of supportive care in intensive care units. Ventricular drainage should be considered in all stuporous or comatose patients with intraventricular haemorrhage and acute hydrocephalus. Given the lack of benefit seen in a the recent STICH trial, emergency surgical evacuation within 72 h of onset should be reserved for patients with large (>3 cm) cerebellar haemorrhages, or those with large lobar haemorrhages, substantial mass effect, and rapidly deteriorating condition.

left CN3, 4,5-1, or 6 palsy

NPC patient with left eye ocular motor palsy, left ptosis
dysarthria, dysphagia
chart 3716182

HACE vergetative resurection

青海高原
塊肉餘生
白菜復活
翠玉如新
the rate of ascend
the prevention recommendation

NE New York University School of Medicine

The Precise Neurological Exam

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General Appearance
Have the patient sit facing you on the examining table. Take a few seconds to actively observe the patient, and continue to actively observe the patient during the exam.

Level of consciousness. Always begin the exam by introducing yourself to the patient as a tool to evaluate the patient's gross level of consciousness. Is the patient awake, alert and responsive? If not, then the exam may have to be abbreviated or urgent actions may have to be taken.

Personal Hygiene and Dress.
Note the patient's dress. Is it appropriate for the environment, temperature, age or social status of the patient? Is the patient malodorous or disheveled?

Posture and Motor Activity. What posture does the patient assume when instructed to sit on the table? Are there signs of involuntary motor activity, including tremors (resting versus intention, also note the frequency in hertz of the tremor), choreoathetotic movements, fasciculations, muscle rigidity, restlessness, dystonia or early signs of tardive dyskinesia? Chorea refers to sudden, ballistic movements, and athetosis refers to writhing, repetitive movements. Fasciculations are fine twitching of individual muscle bundles, most easily noted on the tongue. Dystonia refers to sudden tonic contractions of the muscles of the tongue, neck (torticollis), back (opisthotonos), mouth, or eyes (oculogyric crisis). Early signs of tardive dyskinesia are lip smacking, chewing, or teeth grinding. Damage to the substantia nigra may produce a resting tremor. This tremor is prominent at rest and characteristically abates during volitional movement and sleep. Damage to the cerebellum may produce a volitional or action tremor that usually worsens with movement of the affected limb. Spinal cord damage may also produce a tremor, but these tremors do not follow a typical pattern and are not useful in localizing lesions to the spinal cord.

Height, Build and Weight.
Is the patient obese or cachectic? If cachectic, note any wasting of the temporalis muscles. Note the general body proportions and look for any gross deformities. Also check for dysmorphic features, including low set ears, wide set eyes, small mandible, mongoloid facies, etc.

Vital Signs.
These include temperature, pulse, respiratory rate and blood pressure. It is essential that the vitals always be taken as an initial assessment of a patient. Emergency measures may have to be taken for drastically abnormal vital signs.

Follow this vital sign acquisition routine:

Place the thermometer under the patient's tongue and instruct the patient to keep it there. Wait 20-30 seconds for the results.

Next, find the radial pulse in the patient's right arm with your first two fingertips of your right hand. Look at your watch and count the pulses over 15 seconds and then multiply by 4. Note the quality of the pulse. Is it bounding or thready, weak or prominent, regular or irregular, slow or rapid?. Once you are finished with the pulse measurement, keep your fingers on the pulse and secretly look at the patient's chest and count respirations for 15 seconds and also multiply this number by 4. Keeping your hand on the patient's pulse prevents the patient from becoming conscious of you watching them breath, preventing a likely adjustment in their respiratory rate.

Next, take the blood pressure. If it is high repeat the measurement later in the examination.

Finally, if a high temperature is present, or a previous history was taken suggesting meningeal irritation, test the patient for meningismus. Ask the patient to touch their chin to their chest to evaluate neck stiffness (a person with meningeal inflammation can only do this with pain). A positive Brudzinski's test is when the patient lifts their legs off the table in an effort to releave pain felt when the neck is flexed.

Next, have the patient lie flat on the examining table. Keeping the lower leg flexed, raise the upper leg until it is perpendicular to the floor. Slowly extend the lower leg while keeping the upper leg stationary. If meningeal irritation is present, this maneuver will be painful for the patient. Sometimes the patient will raise their head off the table and/or scream if pain is present, this is considered a positive Kernig's test. Meningismus consists of fever, clouding of consciousness, photophobia (bright light being painful to look at), nuchal rigidity, a positive Brudzinski's test, and possibly a positive Kernig's test.

Special Topic: Classic Cerebrospinal Fluid Characteristics

Idiopathic Seizures	Clear CSF with normal protein, normal glucose, no WBC's, no RBC's, normal opening pressure and normal % Gamma globulin.
Bacterial Meningitis:	Milky CSF with increased protein, decreased glucose, high WBC's (PMN predominate), few RBC's, mildly increased opening pressure and normal % Gamma globulin.
Guillain-Barre Syndrome:	Yellow CSF with very high protein (up to a gram), normal glucose, no WBC's, no RBC's, normal opening pressure and normal % Gamma globulin.
Subarachnoid Hemorrhage:	Yellow CSF with increased protein, normal glucose, few WBC's, inumerable RBC's, mildly increased opening pressure and normal % Gamma globulin.
Herpes Simplex Encephalitis:	Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominate), few RBC's, increase in opening pressure and normal % Gamma globulin.
Viral Meningitis:	Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominate), no RBC's, normal opening pressure and normal % Gamma globulin.
Multiple Sclerosis:	Clear CSF with mild increase in protein, normal glucose, few WBC's (lymphocytic predominate), no RBC's, normal opening pressure, increased % Gamma globulin.
Benign Intracranial Hypertension:	Clear CSF with normal protein, normal glucose, no WBC's, no RBC's, increased opening pressure and normal % Gamma globulin.

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