*alzeimers --social functioning and personality preserved till the later in the disease
*picks disease--personality detereorates early
*prion/crefelt jacobs disease--rapid progression,with myoclonic jerks.
*parkinsons/lewy body dementia--delerium like,waxing and wanning.
-TIA: -EMBOLIC-usually young(look for long travel-transatlantic flight as a clue),affects different regions of brain in different attacks,seen with atrial fibrillation,other heart disese-(valvular,endocardiac,arrhythmias.)
-do ekg followed by transthoracic echocardiogram.
-TR-heparin and warffarin.
-atherothrombotic--
-older person reccurent, stereotyped and shorter in duration
-risk factors of atherosis found(hypert,.DM
,hypercholesterolemia etc)
-mri/ct angiogram for demonstration of stenosis of carotids or low flow
-antiplatelets=aspirin--clopidogril--ticlopidine in this order based on response of patient
*amaurosis fugax:-painless loss of vision from en\mboli
-warning sign of impending stroke
-emboli most commonly from carotid bifurcation
-duplex ultrasound of neck
TOPOGRAPHY OF LESIONS IN STROKE PATIENTS:
*post. limb of internal capsule-motor involment without higher cortical dysfunction or visual field defects.
*middle cerebral artery-contralat.hemiplegia,conjugate eye movement towards infarct side,hemianesthesia,homonemous hemianopeia,aphasi if dominant lobe and hemineglect if nondominant hemisphere involved
*post cerebral at-homonemous hemianopi,alexia without agraphia(dominant hemisphere),visual hallusinations(calcarine cortex),sensory symptoms(thalamus)3 nr palsywith paresis of vertical eye movement and motor defecits(midbrain)
*vertebrobasilar sys.-alternate syndromes(contra hemiplegia with ipsilat cranial nerve involvement)
*lacunar infarcts-pure motor hemiparesis,pure sensory stroke,dysartria,clumpsy hand,ataxic hemiparesis
*thalamus-sensory loss of one half of face with same half body sensation lost.
*medial medularu synd/vertibral artery-contralat arm,leg paralysis with contr loss of tactile,vibratoryand position sense,tounge deviated to injured side
*lateral medullary synd/wallenber/PICA involvement: -ipsilat horners ,loss of pain and temp on same side of face,weakness of palate,pharynx,vocal cords,cerebellar ataxia and contralat loss of pain an temp of body
*lat pons-impaired sensory and motor function of trigeminal nr with accompanying limb ataxia
*medial pons-ipsilat limb ataxia with contrlat. eye deviation an paralysis of face ,arm and leg
@among all risk factors for strokes hypertension has the strongest assosiation with stroke(4 times as compared to non stroke patients)
GAITfew qustions
*hypokinetic/narrow based-stooped posture,short accelerating steps,shuffling feet that scrapes floor=?
*spastic gait-affected limb extended.and dragged in a semicircular fassion=?
*en-bloc gait-staggering with minimal movement of head=?
*wide based,high stepping,rombergs positive=?
MASS/RING ENHANCING LESION IN AIDS PATIENT: *cerebral toxoplasmosis-most common ring enhancing lesion in aids pt
-mri=small,multiple ,spherical lesions in basal ganglia
-toxoplasma serology nonspecific
*primary CNS lymphoma-second most common
-solitary,weakly enhancing,periventricular
-EBV DNA in CSF very specific.
progressive multifocal leukoencephalopathy-opportunistic infec in immuno
compromised,
-caused by jc virus a human polyoma virus
-predominantly in cerebral cortex ,non ring enhancing no
mass effect
-presents with hemiparesis,disturbance in
speech,vision,gait
CAUSES OF SUBARACHNOID HEMORRAGE:
-rupture of saccular aneurysm-mc(>7mm)
-AV malformation
-extension of primary intracerebral hemorrhage
-amyloid angiopathy(older pepople due to degeneration of arteriolar walls)
CAROTID ARTERY STENOSIS
-asymptomatic with 60to99%stenosis benefit from carotid endarterectomy
-<60% followed every 6-12months with carotid dulex ultrasound,surgery not indicated
100%stenosis is contraindication for surgery
CSF IN MULTIPLE SCLEROSIS
- done when mri(most sensitive)is equivocal
-normal pressure,total cell count,total protien but igG elevated(oligoclonal band)
-predominant cells are lymphocytes.
MIGRAINE A/C ATTACK TREAMENT
-simple analgesics(NSAIDS)-->triptans(sumatriptan,razitriptan..)--->ergotamines
order in which drugs are preffered
-triptans prefferd over ergots as few sideeffects
-ergots prefferd if attsck>48hrs or are recurrent,but can cause rebound headache and vascular occlusion hence avoided in chd pts,hypertensives,peripheral vascular disease
-propranal and verapamil used in prophylaxis
PSEUDODEMENTIA
-memory loss in severly depressed elderly person
-easly confussed with alzhiemers
-dexamethsone suppression test used ro differentiate bt dementia and pseudodementia it will be abnormal in 50%of depresed /pseudodem.pt .
-pseudodemented persons are very much conserned about their memory loss and it is thet themselves who come to clinic where as in alzhemers pt is brought in by family members.
-can be reversed with SSRIs for depression
SYRINGOMYELIA
-areflexic weakness in upper extremetiesand dissociated anessthesia(loss of pain and temperature with presserved position and vibration)in a cape distribution.
-cavitary expantion and destruction of grey and white matter adjacent to central canal.
-MC site=lower cervical and upper thoracic.
-if extends into medulla=syringobulbia
-some times associated with arnold-chearri malformation(caudal displacement of fourth ventricle and cerbellar tonsils)
ACOUSTIC NEUROMA
-gradually developing hearing loss and tinnitus
-MRI with gadolinium enhancement
-if associated with multiple cafe au lait spots=neurofibromatosis type II and acoustic neuroma is bilateral in these patients.-surgery
PSEUDOTUMORCEREBRI/benign intrcranial hypertention
-young obese female with headache,absent neurological signs except papilledema and sometimes 6 nr palsy-neuroimaging normal but csf pressure elevateed
-provoking agents=steroids,ocps,vitA..-impaired absorption of csf by arachnoid villi
-RX-=weight reduction,acetazolamide if no releiff then shunting or optic nr fenestration to releive pressure which otherwise leads to blindness as complication
-
*normal pressure hydrocephalus-triad of ataxia,urinary incontinence and dementia,enlarged ventricles on ct,shunting as treatement.
*petitmal seizures-sudden cessation of mental activity for very short time but frequent,no automatisms or tonic-clonic activity,EEG with activation(hyperventilation,phobic stimulation and sleep)is diagnostic -3hzspike and wavw pattern
Brain cells fused with computer chips
Tests with neurons could lead to better computers, brain treatments
P. Fromherz / NACHIP / Max Planck Institute for Biochemistry
A neuron from a rat brain sprawls over a linear array of transistors. The cell's ionic current interacts with the electronic current in the silicon.
View related photos INTERACTIVE
The line between living organisms and machines has just become a whole lot blurrier. European researchers have developed "neuro-chips" in which living brain cells and silicon circuits are coupled together.
The achievement could one day enable the creation of sophisticated neural prostheses to treat neurological disorders, or the development of organic computers that crunch numbers using living neurons.
To create the neuro-chip, researchers squeezed more than 16,000 electronic transistors and hundreds of capacitors onto a silicon chip just 1 millimeter square in size.
They used special proteins found in the brain to glue brain cells, called neurons, onto the chip. However, the proteins acted as more than just a simple adhesive.
"They also provided the link between ionic channels of the neurons and semiconductor material in a way that neural electrical signals could be passed to the silicon chip," said study team member Stefano Vassanelli from the University of Padua in Italy.
The proteins allowed the neuro-chip's electronic components and its living cells to communicate with each other. Electrical signals from neurons were recorded using the chip's transistors, while the chip's capacitors were used to stimulate the neurons.
It could still be decades before the technology is advanced enough to treat neurological disorders or create living computers, the researchers say, but in the nearer term, the chips could provide an advanced method of screening drugs for the pharmaceutical industry.
"Pharmaceutical companies could use the chip to test the effect of drugs on neurons, to quickly discover promising avenues of research," Vassanelli said.
The researchers are now working on ways to avoid damaging the neurons during stimulation. The team is also exploring the possibility of using a neuron's genetic instructions to control the neuro-chip.
THALAMIC SYNDROME/DYGERINE ROUSSY SYNDROME -caused by stroke involving ventral postero lateral nucleus (VPL-VERY PSYCHOTIC LESION)of thalamus which transmits sensory information from contralateral side of body
-features;contralateral hemianesthesia sometimes hemiparesis,athetosis,ballistic movements.
-dysthesia of affected side is charecteristic=thalamic pain syndrome. isnt this cute
HYPERTENSIVE INTRACEREBRAL HEMMORHAGE
*PUTAMEN-most common site35%,compression of internal capsule-->hemiparesis
-hemisensory loss,homonemoushemianopsia,stupor,coma also occurs
-eyes deviated away from affected side
*CEREBELLAR HEMORRAGE-16%,ataxia ,vomitting,occipital headache,gaze palsy and facial weakness,noo hemiparesis.
-urgent decompression needed to prevent br stem compression
*PONTINE HEMORRAGE-5-12%,PRESENT WITH DEEP COMA AND PARAPLEGIA,within minutes .
-pinpoint pupils reactive to light
-decerebrate rigidity.
MYASTHENIA GRAVIS
-antiacetylcholine receptor antibodies detection preffered test for diagnosis of MG
-tensilon test done but serology is curently done
*yong person with fever,meningial signs positive developing features of shock,petechiae and purpura-->WATERHOUSE-FRIEDRICHSON SYNDROME(DIC following hemorrhage into adrenal glands leading to A/Cadrenal insuffiency
The subclavian steal syndrome may lead to transient vertebrobasilar ischemia. Symptoms develop when there is localized stenosis or occlusion of one subclavian artery proximal to the source of the vertebral artery, so that blood is "stolen" from this artery. A bruit in the supraclavicular fossa, unequal radial pulses, and a difference of 20 mm Hg or more between the systolic blood pressures in the arms should suggest the diagnosis in patients with vertebrobasilar transient ischemic attacks.
Multiple sclerosis: signs and symptoms INSULAR: Intention tremor/internuclear ophtalmoplegia
Nystagmus
Slurred speech
Uthoff's phenomenon=Uhtoff's phenomenon describes the well known finding of a temporary production or worsening of neurological symptoms in MS patients exposed to heat, such as that from a hot shower, exercise, or a warm climate. This is thought to be due to the effect of heat on myelin (insulation sheath or covering of nerves) which results in abnormal transmission of nerve impulses
Lhermitte's sign-flexing of neck produces electric shock sensation running down
the spine
Ataxia
Rebound/relapses
PROGNOSTIC FACTORS IN BREAST CANCER PATIENTS
-Stage of breast cancer/tumor burden Is the most reliable indicator of prognosis
-Patients with disease localized to the breast and no evidence of regional spread sgI,BUT sg IV have worst prognosis.
- Estrogen and progesterone receptors are prognostic variables because patients with hormone receptor-negative tumors and no evidence of metastases to the axillary lymph nodes have a much higher recurrence rate than do patients with hormone receptor-positive tumors and no regional metastases.
- histologic subtype of breast cancer (eg, medullary, lobular, colloid) seems to have little significance in prognosis once these tumors are truly invasive. Flow cytometry of tumor cells to analyze DNA index and S-phase frequency aid in prognosis. Tumors with marked aneuploidy have a poor prognosis
-HER-2/neu oncogene amplification, epidermal growth factor receptors, and cathepsin D may have some prognostic value
Risk of Colon Cancer in ulcerative colitis factors increasing risk;
-disease proximal to the sigmoid colon
-patients who have had colitis for more than 10 years
[i]Factors decreasing the risk[/i]
-. Ingestion of folic acid, 1 mg/d,
-patient undergoingregular Colonoscopies ( recommended every 1–2 years in patients with extensive colitis, beginning 8–10 years after diagnosis.)
At colonoscopy, multiple random mucosal biopsies are taken throughout the colon to look for dysplasia or carcinoma. Because of the relatively high incidence of concomitant carcinoma in patients with dysplasia (either low or high grade) , colectomy is recommended.
Gastric MALT(mucosa associated lmphoid tissue)
-Lymphoma is the second most common gastric malignancy, 3–6% of gastric cancers. More than 95% of these are non-Hodgkin's B cell lymphomas. Gastric lymphomas may be primary (arising from the gastric mucosa) or may represent a site of secondary involvement in patients with nodal lymphomas. About 60% of primary gastric lymphomas are believed to arise from mucosa-associated lymphoid tissue (MALT). -
Because the prognosis and treatment of primary and secondary gastric lymphomas are entirely different, the distinction is important. B cells of nodal origin may be distinguished from those derived from MALT (CD19 and CD20 positive).
-Infection with H pylori may be an important risk factor for the development of primary gastric lymphoma. Chronic infection with H pylori causes an intense lymphocytic inflammatory response that may lead to the development of lymphoid follicles.
-The clinical presentation and endoscopic appearance of gastric lymphoma are similar to those of adenocarcinoma. The majority of patients present with abdominal pain, weight loss, or bleeding. At endoscopy, lymphoma may appear as an ulcer, mass, or diffusely infiltrating lesion. The diagnosis is established with endoscopic biopsy.
-Patients with primary low-grade gastric MALT-lymphoma should be tested for H pylori infection and treated if positive(Omeprazole,claritromycin and amoxicilin). regression after successful H pylori eradication occurs in 75% of cases of low-grade lymphoma.
-if fail to respond to eradication therapy can be treated successfully with surgical resection, local radiation therapy, or combination therapy.
-high-grade lymphomas may be treated with resection and CHOP chemotherapy. .
Whipple's triad
is characteristic of hypoglycemia regardless of the cause. It consists of (1) a history of hypoglycemic symptoms, (2) an associated fasting blood glucose of 40 mg/dL or less, and (3) immediate recovery upon administration of glucose.
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*small cell carcinoma of lung/oat cell ca(small amount urine)
-produces ACTH causing SIADH as paraneoplastic syndr,
*squamous cell ca(sCa++mous)
-produces PTH like substance causing hypercalcemia as paraneoplastic syndr.
__________________________________________________________________
*cause of bleeding in cystic fibrosis patient
-defeceincy of pancreatic ezymes..............>fat malabsorption. ...........>deficency of fat soluble vitamins(A,D,E,K)..........>vitK is required for post translational modificaton of coagulation ftrs II,VII,IX$X as well as proteinC$S.........>DEFECIENT factors.........>bleeding
+
frequent antibiotic usage for recurrent pulmonary infection also predisposes
Monoclonal Gammopathy of Uncertain Significance/MGUS
-M protein(igG,IgM,igA) in the serum without symptoms or signs of multiple myeloma, macroglobulinemia, amyloidosis, or lymphoma.
-Less than 10% plasma cells in the bone marrow.
-No clinical symptoms are associated with MGUS.
--Lymphoid malignancies, amyloidosis, or multiple myeloma will develop in one-third of patients with apparently benign monoclonal gammopathies.
- No specific therapy is necessary, but close observation is required. -
-MGUS patients should be periodically monitored for changes in serum M proteins, urinary Bence-Jones proteins, evidence of renal failure, anemia, hypercalcemia, lytic bone lesions, or bone marrow plasmacytoses.
Other Diseases of Immunoglobulin Overproduction (Gammopathies)
.-Multiple Myeloma
-Waldenström's Macroglobulinemia
-Amyloidosis( only primary amyloidosis (AL), the protein fibrils are monoclonal immunoglobulin light chains,whereas in secondary amyloidosis (AA), protein deposits are derived from acute phase reactant apolipoprotein precursors)
Juvenile Angiofibroma
- Any adolescent male with nasal mass ,recurrent epistaxishighly vascular tumors-bleed on touch) should be considered angiofibroma until proven otherwise.
- cause nasal obstruction and hemorrhage. are benign, but these tumors expand locally .
- Treatment consists of preoperative embolization followed by surgical excision . Small angiofibromas may be resected endoscopically. Extensive ones may require skull base approaches.
-Recurrences are common and should be resected if possible.
Other Benign Nasal Tumors
-Nasal Polyps=pale, edematous, mucosally covered masses commonly seen in patients with allergic rhinitis
-Inverted Papilloma=are benign tumors that usually arise in the common wall between the nose and maxillary sinus. They present with unilateral nasal obstruction and occasionally hemorrhage.
-chondroma of nasal cartiledge
other causes of nasal bleed
-foreign body (in child)
-cocaine abuse
-bleeding disorder
THINGS TO REMEMBER ABOUT IN Chronic Myelogenous Leukemia
-Strikingly elevated white blood count.
-Markedly left-shifted myeloid series
-Presence of Philadelphia chromosome or bcr/abl gene.( The fusion gene bcr/abl produces a novel protein that differs from the normal transcript of the abl gene in that it possesses tyrosine kinase activity)
-Phases in CML:-Early CML /chronic phase- doest behave like a malignant disease. Normal bone marrow function is retained, the neutrophils combat infection normally.
-accelerated phase
- finally after several years, to blast crisis.
-Ocassionally patient will present with a clinical syndrome related to leukostasis with blurred vision, respiratory distress, or priapism. The white blood count in these cases is usually greater than 500,000/mcL.
-bcr/abl gene is detected in the peripheral blood by the polymerase chain reaction (PCR) test, which has now supplanted cytogenetics in looking for the Philadelphia chromosome.
-RX= imatinib mesylate/Gleevec- inhibitor of the tyrosine kinase activity of the bcr/abl oncogene.. It has now replaced both interferon and hydroxyurea as standard therapy. The most common toxicities are nausea, periorbital swelling, edema, rash, and myalgia, but most of these are modest.
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and sometimes 6 nr palsy
and dementia,enlarged ventricles on ct,shunting as treatement.
-caused by stroke involving ventral postero lateral nucleus (
isnt this cute
,vomitting,occipital headache,gaze palsy and facial weakness,noo hemiparesis.
for diagnosis of MG
