case study

http://www.umassmed.edu/strokestop/dataviews/caseindex.html

brainstem

3 parts:

1. Ventral: contains motor pathways
2. middle: contains sensory pathway
3. dorsal: contains Cranial nerve nuclei

- Muscles of mastication and forehead muscles have bilateral supply while facial muscle  have unilateral supply .

-crossed sensory loss : lesion is between mid pons and c2 level. 

cerebeller lesion, cranial nerve lesion are ipsilateral, cr

neuro Differential diagnosis

http://books.google.com/books?id=tnah3LN7XmcC&pg=PP1&dq=john+patten+neurological#v=onepage&q=john%20patten%20neurological&f=false

Rule of 4 for brainstem lesion

http://lifeinthefastlane.com/wp-content/uploads/2011/06/Rule_of_4_Brainstem1.pdf?9d7bd4

http://lifeinthefastlane.com/wp-content/uploads/2011/07/Rule-of-4-Illustration-Tor-Ercleve.jpg?9d7bd4

http://lifeinthefastlane.com/2009/05/using-the-brainstem-2/

clinical Case

http://lifeinthefastlane.com/education/clinical-cases/

HOw to read ct brain

http://www.neurosurvival.ca/ComputerAssistedLearning/readingCTs/how_to_read_a_ct_image.htm

Localisation of lesion

http://lifeinthefastlane.com/2009/05/brainstem-rules-of-4/

Images:
http://rad.usuhs.edu/medpix/kiosk_image.html?mode=&imid=37944&pt_id=11166&quiz=no&page=&th=&map=&skiprows=&this_week=&skipcases=0&maxcases=5&sth=-1#pic

stroke evolution

• Hyperacute: <6 hours: best described as cytotoxicoedema represented by the shift of waterin neurons. Because this is a relatively modest change, the CT in this stage is usually negative. On occasion, a CT scan obtainedin the hyperacute phase can give direct signs(e.g., vessel hyperdensity, subtle parenchymalhypodensity) or indirect signals (e.g., sulcaleffacement, gyral swelling, ventricular compression,fading of the white matter/grey matter interface)of hyperacute ischaemia. Such findingshave a negative prognostic value and are directlyassociated with the degree of neurological disability. Vessel hyperdensity in major cerebralarteries or one of their branches (the middlecerebral artery is the most commonly affected)can be observed within the first minutes following the onset of neurological signs andsymptoms and takes place before the appearanceof CT findings of the parenchymal infarct inthe corresponding territory. This increasein intravascular density, which is visible on CT without the use of contrast agents, appearsto be caused by the formation of an endoluminalclot, either by arterial thrombosis orembolism

Acute: – The acute phase of ischaemia occurs within the first 24 hours of the event, but typically begins within 6 hours after the stroke onset. From a neuropathological point of view, vasogenic oedema is present as supported by the filling of the extracellular spaces of the brain due to a blood-brain barrier breakdown. 

Subacute:  

24 hours after the event and continues until six weeks from the onset. From a neuropathological

point of view, beginning in the start of the second week there is an increase in   the vasogenic oedema as  in CT by an area with increasingly low attenuation coefficients, better defined margins and mass effect (internal cerebral herniations are possible,especially in cases of massive ischaemia) the ischaemic area appears most clearlytwo to three days after clinical onset of stroke.From the second week after the event, the oedemaand mass effect gradually subside and the area of hypodensity becomes less clear in some cases it disappears altogetherand the ischaemic area becomes difficultor impossible to distinguish from the normalbrain surrounding it. This is the so-called“fogging effect”, which is supported neuropathologicallyby an increase in cellularity dueto the invasion of microphages and the proliferation of capillaries 

Chronic: the chronic stage of ischaemiacoincides with the start of the sixth week from the onset of the clinical stroke and ischaracterized by repair processes. Parenchyma lhypodensity with well-defined marginsappears with attenuation values in the CSF range

Neuroradiology book

http://books.google.com/books?id=uH0R1SX7b0IC&printsec=frontcover&dq=neuroradiology&hl=en&ei=TSNoTt_AKoSCgAfQ0ezrDA&sa=X&oi=book_result&ct=result&resnum=5&sqi=2&ved=0CD4Q6AEwBA#v=onepage&q=stroke&f=false


http://books.google.com/books?id=bR6YTH1fycUC&printsec=frontcover&dq=neuroradiology&hl=en&ei=TSNoTt_AKoSCgAfQ0ezrDA&sa=X&oi=book_result&ct=result&resnum=6&sqi=2&ved=0CEQQ6AEwBQ#v=onepage&q&f=false

how to read brain MRI

http://www.med.wayne.edu/diagradiology/anatomy_modules/brain/brain.html

http://www.med.harvard.edu/aanlib/cases/caseNA/pb9.htm


https://www.msu.edu/~brains/brains/human/index.html

spinal stenosis

http://www.youtube.com/watch?v=WGY6GDJUBPY&NR=1

How to read Spine MRI

Cervical Spine MRI
http://www.youtube.com/watch?v=iyWEXDSt7xY&NR=1

http://www.youtube.com/watch?v=9n09uGsCEkA&NR=1
http://www.youtube.com/watch?v=SwNF_foFfAQ&feature=related

lumbar spine MRI
http://www.youtube.com/watch?v=C9LBdAwBVZg&feature=related
http://www.youtube.com/watch?v=PZqimf1DbcE&feature=related

MRI basics

What is MRI??
MAgnetric resonance Imaging: When we apply magnetic field --> Hydrogen from water molecule starts moving in direction of Field ,rate of spin depends  on strength of magnetic field ...now if you remove magnetic field --> Hydrogen will try to come back to normal ...

In a typical T₁-weighted image, water molecules in a sample are excited with the imposition of a strong magnetic field. This causes many of the protons in water molecules to precess simultaneously, producing signals in MRI. In T₂-weighted images, contrast is produced by measuring the loss of coherence or synchrony between the water protons. When water is in an environment where it can freely tumble, relaxation tends to take longer. In certain clinical situations, this can generate contrast between an area of pathology and the surrounding healthy tissue.
spinning will produce contarst---faster in free flowing water like Ventricle...while slower in gret-white matter.while negligible in bone

Diffusion weighted MRI:
In diffusion-weighted images, instead of a homogeneous magnetic field, the homogeneity is varied linearly by a pulsed field gradient. Another gradient pulse is applied in the same direction but with opposite magnitude to refocus or rephase the spins. The refocusing will not be perfect for protons that have moved during the time interval between the pulses, and the signal measured by the MRI machine is reduced. This reduction in signal due to the application of the pulse gradient can be related to the amount of diffusion that is occurring.
The first successful clinical application of DWI was in imaging the brain following stroke in adults. Areas which were injured during a stroke showed up "darker" on an ADC map compared to healthy tissue. At about the same time as it became evident to researchers that DWI could be used to assess the severity of injury in adult stroke patients, they also noticed that ADC values varied depending on which way the pulse gradient was applied. This orientation-dependent contrast is generated by diffusion anisotropy, meaning that the diffusion in parts of the brain has directionality. This may be useful for determining structures in the brain which could restrict the flow of water in one direction, such as the myelinated axons of nerve cells (which is affected by multiple sclerosis). However, in imaging the brain following a stroke, it may actually prevent the injury from being seen. To compensate for this, it is necessary to apply a mathematical operator, called a tensor, to fully characterize the motion of water in all directions.
Diffusion-weighted images are very useful to diagnose vascular strokes in the brain. It is also used more and more in the staging of non small cell lung cancer, where it is a serious candidate to replace positron emission tomography as the 'gold standard' for this type of disease. Diffusion tensor imaging is being developed for studying the diseases of the white matter of the brain as well as for studies of other body tissues


FLAIR:
Fluid Attenuated Inversion Recovery (FLAIR)^[27] is an inversion-recovery pulse sequence used to null signal from fluids. For example, it can be used in brain imaging to suppress cerebrospinal fluid (CSF) so as to bring out the periventricular hyperintense lesions, such as multiple sclerosis (MS) plaques. By carefully choosing the inversion time TI (the time between the inversion and excitation pulses), the signal from any particular tissue can be suppressed

neural foraminal stenosis

stroke cases

http://www.strokecenter.org/education/ais_ct_tool/index.htm

Case discussion

http://library.med.utah.edu/neurologicexam/cases/home_cases.html

A 57-Year-Old Man With an Abnormal Right Eye and Left Hemiparesis

very interesting case of of Internal carotid artery dissection from Medscape...

A 57-year-old man presents to the emergency department with left-sided facial, arm, and leg weakness along with slurred speech after suffering violent and repetitive bouts of coughing. His wife has the impression that his right eye is smaller than the left. The patient also complains of pain over his right eye. His medical history is notable for hypertension and smoking 1 pack of cigarettes per day for 10 years. He denies any illicit drug use. He does not consume alcohol. He is employed, does not exercise, and has a sedentary lifestyle. There is no history of previous head or neck injury.

On physical examination, his oral temperature is 97.3°F (36.3°C). His pulse is regular with a rate of 94 bpm. His blood pressure is 195/105 mm Hg. The examination of his head and neck is normal. His lungs are clear to auscultation and have normal respiratory effort. No cardiac murmurs are detected. His abdomen is soft and nontender, with normal bowel sounds on auscultation. On neurologic examination, the patient is alert and oriented to time and place. His speech is slurred and dysarthric. On cranial nerve examination, the right pupil constricts from 2 mm to 1.5 mm in response to light, whereas the left pupil constricts from 3 mm to 2 mm. The right eyelid has 3 mm of ptosis compared with the left eye, and the right eye appears to be smaller than the left one. Pupillary asymmetry is more apparent when lights in the room are dimmed. Funduscopic examination reveals normal fundi. Visual acuity is normal bilaterally. The extraocular movements are intact. Facial sensation is decreased to light touch and pinprick on the left side. The patient has a decreased left nasolabial fold. He has weak movements of the left side of the face, without forehead involvement. The gag reflex is present, and there is normal palate elevation. After pinching the left side of the neck, the left pupil dilates normally (ciliospinal reflex). After pinching the right side of the neck, the right pupil does not dilate. He is unable to stand and walk. Muscular tone is flaccid on the left side but normal on the right. He has a marked left hemiparesis. The patient's reflexes are normal throughout except for an up-going plantar response on the left side, compared with a down-going one on the right. The patient reports decreased sensation to light touch, temperature, pinprick, joint position, and vibration on the left half of the body. His National Institute of Health Stroke Scale (NIHSS) is 11.

Routine laboratory analyses are performed and result normal. Chest x-ray is normal. ECG shows left ventricular hypertrophy. A noncontrast CT scan of the head reveals a hyperdense right middle cerebral artery (Figure 1).

Conventional angiography reveals stenosis at the origin of right internal carotid artery, with an abrupt narrowing of its lumen ("rattail-filling defect"; Figure 2).

he patient in this case presented with a pattern of sensory loss and weakness on the left side of his body consistent with a lesion involving the right corticospinal and corticobulbar fibers and the primary somatosensory cortex. The most likely diagnosis was an ischemic stroke. Neurologic examination also revealed ptosis of the right eye with narrowing of the palpebral aperture, miosis in the right eye with a pupil that was reactive to light, and reduced ciliospinal reflex on pinching the right side of the neck. These signs are consistent with a partial Horner syndrome resulting from injury to sympathetic fibers traveling with the internal carotid artery. The sudden onset of neurologic deficits after violent coughing and the presence of pain over the patient's right eye are highly suggestive of a right internal carotid artery dissection. Conventional angiography was performed because the clinical findings were highly suspicious for an internal carotid artery dissection; this confirmed the diagnosis by showing an abrupt narrowing of the vessel's lumen ("rattail-filling defect"). The hyperdense middle cerebral artery revealed by noncontrast CT scan of the head suggested an occlusion of this artery. Laboratory analysis performed during hospitalization revealed the presence of mild hyperlipidemia. Screening analyses for hypercoagulability and rheumatologic disorders were normal. Transthoracic echocardiography was normal; however, duplex ultrasonographic imaging showed a stenosis in the right internal carotid artery.

Dissection of the internal carotid artery is an important cause of cerebrovascular disease in young adults. One study out of Rochester, Minnesota, showed an annual incidence of 2.6 patients out of 100,000 population. The actual incidence is difficult to evaluate, however, and may be higher because this condition, which may be asymptomatic or have various clinical presentations, may go unrecognized.^[1] The incidence appears to have increased since the 1980s, but is likely due to the availability of better imaging studies.^[1]

Dissection normally occurs in the extracranial segment of the epiaortic vessels. The internal carotid artery is affected more often than the vertebral artery.^[2] Dissections can be classified as traumatic or spontaneous. Traumatic dissections are linked to direct neck trauma or injury, whereas spontaneous dissections may be secondary to predisposing factors, such as fibromuscular dysplasia, Ehlers-Danlos syndrome, cystic medial necrosis, or Marfan syndrome. These conditions cause an abnormal, weakened arterial wall, thus predisposing patients to arterial dissection.^[3]

Internal carotid artery dissection develops as a consequence of a tear in the intimal layer of the vessel, which allows blood to enter the wall of the artery and to split its layers, which is termed a subintimal hematoma. This means that the hematoma is located between the intimal and medial layers of the artery. Alternatively, a rupture of the vasa vasorum causes a subadventitial hematoma (ie, a hematoma between the media and the adventitial layers). Internal carotid artery dissection can lead to thrombus formation and the risk for distal embolization, whereas arterial narrowing with stroke due to inadequate blood flow is a less common mechanism of ischemia.^[4]Hematoma formation and a localized inflammatory response result in compression of nearby structures, such as the sympathetic fibers of the superior cervical ganglion, which lies in the posterior wall of the carotid sheath. This can cause a postganglionic oculosympathetic palsy. There is no anhidrosis because sweat fibers run with the uninvolved external carotid artery.

The most typical signs and symptoms of internal carotid artery dissection are neck pain and/or a partial Horner syndrome. This may be followed by an ischemic event ipsilateral to the ocular signs, with somatosensory and/or motor deficits contralateral to ocular signs as a consequence of distal embolization to the intracerebral arteries.

A highly suggestive constellation of signs and symptoms frequently seen with internal carotid artery dissection is Horner syndrome. Oculosympathetic palsy in the form of Horner syndrome has long been recognized as a typical manifestation of internal carotid artery dissection, although it is found in fewer than half of patients. The classic signs of Horner syndrome are ptosis of the upper lid, slight elevation of the lower lid (upside-down ptosis), and miosis reactive to light. The narrow palpebral aperture secondary to upper-lid ptosis and elevation of the lower lid give the illusion that the affected eye is smaller than the contralateral eye (illusory enophthalmos). Horner syndrome is an expression of a disruption of oculosympathetic pathways. Ptosis (ie, upper eyelid droop) is caused by a loss of innervation to Müller's smooth muscle in the upper lid. This small muscle is innervated by sympathetic fibers and is responsible for eye opening, together with the superior and levator palpebrae: striated skeletal muscle innervated by the third cranial nerve. Similarly, miosis (ie, decreased papillary size) is caused by a loss of sympathetic innervation to the iris pupillodilator muscle. As a consequence, the pupil cannot dilate. This impaired dilation of the pupil may also be observed in a test of the ciliospinal reflex. Normally, pinching the neck causes a papillary dilation secondary to the activation of sympathetic pathway. In an eye with Horner syndrome, this dilation does not occur.

Currently, the most commonly available imaging modalities are carotid ultrasonography and CT angiography (CTA) of the head and neck. However, the best method to diagnose an internal carotid artery dissection is a combination of CTA and magnetic resonance angiography (MRA) with fat-suppressed T1 images.^[1,5,6] CTA and MRA are replacing conventional angiography in the diagnosis of internal carotid and vertebral artery dissection because the resolution and accuracy of CTA and MRA are similar to that of angiography.^[7-9] Moreover, MRI may show the intramural hematoma itself. As an alternative, conventional angiography with digital subtraction may be used, although these tests are more expensive and invasive than MRI/MRA. Additionally, MRI/MRA is superior to conventional angiography in diagnosing dissections without associated luminal abnormalities.^[1] Conventional angiography may reveal an abrupt narrowing of the internal carotid artery lumen (rattail-filling defect or the "string sign"). Carotid duplex ultrasonographic imaging may also be useful, especially in the younger population, with less chance of severe atherosclerotic disease, which can interfere in the diagnosis.^[10] Direct observation of a luminal intimal flap is diagnostic but rare; the most frequent finding is a stenosed or occluded vessel in the absence of atheromatous lesions.^[11,12]

The treatment of internal carotid artery dissection consists of anticoagulation with intravenous heparin followed by oral anticoagulation for 3-6 months.^[13] However, there are no randomized controlled trials supporting such a therapeutic approach, and the validity of such treatment has never been definitively proven.

The patient in this case was first treated with intravenous heparin followed by oral anticoagulation in order to prevent distal embolization. He continued anticoagulant therapy for 3 months. The patient's Horner syndrome resolved completely after 3 days, but the left-sided sensorimotor deficits persisted at discharge.

Effect of fructose/corn syrup vs glucose on ur brian....

Brain activity in the hypothalamus, one brain area involved in regulating food intake, was not affected by either fructose or glucose. However, activity in the cortical brain control areas showed the opposite response during infusions of the sugars. Activity in these areas was inhibited when fructose was given but activated during glucose infusion.

This is an important finding because these control brain areas included sites that are thought to be important in determining how we respond to food taste, smells, and pictures, which the American public is bombarded with daily.

"This study provides evidence in humans that fructose and glucose elicits opposite responses in the brain. It supports the animal research that shows similar findings and links fructose with obesity," added Purnell.

"For consumers, our findings support current recommendations that people be conscious of sweeteners added to their drinks and meals and not overindulge on high-fructose, processed foods."

Evolution of the female brain: From biology to behaviour

Female and male brains evolved differently to help ensure survival of the species. In ancient times, each sex had a very defined role: Cavemen hunted; cavewomen nurtured the family. Specific brain areas perhaps sharpened to enable each sex to carry out their jobs. Interest and research on sex differences in the brain especially increased over the past two decades. It emerged that while there are more similarities than differences in the brain structure, function and brain chemicals (neurochemicals) between healthy women and men, there are important differences that distinguish the female from the male brain. Women and men think, feel, perceive and behave differently; socialization alone does not account for all of it.

Women have more brain circuits for communication, reading emotions , social nuances, nurturing skills and a greater ability to use both sides of the brain simultaneously, although the number of brain cells in women and men is the same. Women are, on an average, better at expressing emotions and remembering details of emotional events (hippocampus—the hub of emotion and memory is larger in a woman's brain).

Women are better at reading faces and recognizing emotional overtones in others (face coding is bilateral in the female brain). This may also account for some wellknown feminine intuitive abilities.

The outstanding verbal agility of women is undebatable! A significant proportion of the female verbal advantage can be attributed to a larger area of the female brain devoted to language. Yale Universityresearchers showed the brain of women processes verbal language simultaneously on both sides unlike in men.

Women's brain is better able to multi-focus, hence multi-task , a talent that has helped them juggle a home, career and social responsibilities . Some researchers attribute this to a differently shaped corpus callosum—the area connecting the two sides of the brain—and to a greater ability to use both simultaneously.

Women and men are differently sensitive to stress, conflict and the perception of pain; distinct sex-specific differences in neurochemicals such as dopamine, serotonin and gamma-aminobutyric acid contribute towards this difference.

Jill Bolte Taylor's stroke of insight | Video on TED.com

Jill Bolte Taylor's stroke of insight | Video on TED.com

VS Ramachandran on your mind

VS Ramachandran on your mind | Video on TED.com

vASCULITIS

Case: MRI brain, 2/21/96, 2/28/96, & Cerebral Angiogram, 2/22/96: CNS Vasculitis with evidence of ischemic infarction in the right and left frontal lobes. CC: Difficulty with word finding. Hx: This 27y/o RHF experienced sudden onset word finding difficulty and slurred speech on the evening of 2/19/96. She denied any associated dysphagia, diplopia, numbness or weakness of her extremities. She went to sleep with her symptoms on 2/19/96, and awoke with them on 2/20/96. She also awoke with a headache(HA) and mild neck stiffness. She took a shower and her HA and neck stiffness resolved. Throughout the day she continued to have difficulty with word finding and had worsening of her slurred speech. That evening, she began to experience numbness and weakness in the lower right face. She felt like there was a "rubber-band" wrapped around her tongue. For 3 weeks prior to presentation, she experienced transient episodes of a "boomerang" shaped field cut in the left eye. The episodes were not associated with any other symptoms. One week prior to presentation, she went to a local ER for menorrhagia. She had just resumed taking oral birth control pills one week prior to the ER visit after having stopped their use for several months. Local evaluation included an unremarkable carotid duplex scan. However, a HCT with and without contrast reportedly revealed a left frontal gyriform enhancing lesion. An MRI brain scan on 2/20/96 revealed nonspecific white matter changes in the right periventricular region. EEG reportedly showed diffuse slowing. CRP was reportedly "too high" to calibrate. MEDS: Ortho-Novum 7-7-7(started 2/3/96), and ASA(started 2/20/96). PMH: 1)ventral hernia repair 10 years ago, 2)mild "concussion" suffered during a MVA; without loss of consciousness, 5/93, 3) Anxiety disorder, 4) One childbirth. FHx: She did not know her father and was not in contact with her mother. SHx: Lives with boyfriend. Smokes one pack of cigarettes every three days and has done so for 10 years. Consumes 6 bottles of beers, one day a week. Unemployed and formerly worked at an herbicide plant. EXAM: BP150/79, HR77, RR22, 37.4C. MS: A&O to person, place and time. Speech was dysarthric with mild decreased fluency marked by occasional phonemic paraphasic errors. Comprehension, naming and reading were intact. She was able to repeat, though her repetition was occasionally marked by phonemic paraphasic errors. She had no difficulty with calculation. CN: VFFTC, Pupils 5/5 decreasing to 3/3. EOM intact. No papilledema or hemorrhages seen on fundoscopy. No RAPD or INO. There was right lower facial weakness. Facial sensation was intact, bilaterally. The rest of the CN exam was unremarkable. MOTOR: 5/5 strength throughout with normal muscle bulk and tone. Sensory: No deficits. Coord/Station/Gait: unremarkable. Reflexes 2/2 throughout. Plantar responses were flexor, bilaterally. Gen Exam: unremarkable. COURSE: CRP 1.2(elevated), ESR 10, RF 20, ANA 1:40, ANCA <1:40, TSH 2.0, FT4 1.73, Anticardiolipin antibody IgM 10.8GPL units(normal <10.9), Anticardiolipin antibody IgG 14.8GPL(normal<22.9), SSA and SSB were normal. Urine beta-hCG pregnancy and drug screen were negative. EKG, CXR and UA were negative. MRI brain, 2/21/96 revealed increased signal on T2 imaging in the periventricular white matter region of the right hemisphere. In addition, there were subtle T2 signal changes in the right frontal, right parietal, and left parietal regions as seen previously on her local MRI can. In addition, special FLAIR imaging showed increased signal in the right frontal region consistent with ischemia. She underwent Cerebral Angiography on 2/22/96. This revealed decreased flow and vessel narrowing the candelabra branches of the RMCA supplying the right frontal lobe. These changes corresponded to the areas of ischemic changes seen on MRI. There was also segmental narrowing of the caliber of the vessels in the circle of Willis. There was a small aneurysm at the origin of the LPCA. There was narrowing in the supraclinoid portion of the RICA and the proximal M1 and A1 segments. The study was highly suggestive of vasculitis. 2/23/96, Neuro-ophthalmology evaluation revealed no evidence of retinal vasculitic change. Neuropsychologic testing the same day revealed slight impairment of complex attention only. She was started on Prednisone 60mg qd and Tagamet 400mg qhs. On 2/26/96, she underwent a right frontal brain biopsy. Pathologic evaluation revealed evidence of focal necrosis(stroke/infarct), but no evidence of vasculitis. Immediately following the brain biopsy, while still in the recovery room, she experienced sudden onset right hemiparesis and transcortical motor type aphasia. Initial HCT was unremarkable. An EEG was consistent with a focal lesion in the left hemisphere. However, a 2/28/96 MRI brain scan revealed new increased signal on T2 weighted images in a gyriform pattern from the left precentral gyrus to the superior frontal gyrus. This was felt consistent with vasculitis. She began q2month cycles of Cytoxan(1,575mg IV on 2/29/96. She became pregnant after her 4th cycle of Cytoxan, despite warnings to the contrary. After extensive discussions with OB/GYN it was recommended she abort the pregnancy. She underwent neuropsychologic testing which revealed no significant cognitive deficits. She later agreed to the abortion. She has undergone 9 cycles of Cytoxan( one cycle every 2 months) as of 4/97. She had complained of one episode of paresthesias of the LUE in 1/97. MRI then showed no new signs ischemia.

Cellphones and Brian

This study says spending 50 min with your cellphone close to ear is enough to alter Glucose  metabolism showing increased brain activity in part of brain closest to antenna. SO weak electromagnetic radiation does have an effect on brain


Volkow's team studied 47 people who had brain scans while a cellphone was turned on for 50 minutes and another while the phone was turned off. While there was no overall change in brain metabolism, they found a 7% increase in brain metabolism in the region closest to the cellphone antenna when the phone was on. As Volkow notes at the end of the Nytimes article, this may lead to the discovery of a mechanism for brain stimulation. Right now they don’t know what the mechanism is by which the electromagnetic field is causing the glucose metabolism. If neuronal firing is being altered, and if the bandwidth turns out to be sufficiently high (i.e. if the stimulation can be made sufficiently precise), this could eventually lead to a wireless brain-machine in

Nora D. Volkow, Dardo Tomasi, Gene-Jack Wang, Paul Vaska, Joanna S. Fowler, Frank Telang, Dave Alexoff, Jean Logan, Christopher Wong. Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. JAMA. 2011;305(8):808-813.



One more study done at IIT-Mumbai and telecom sector says dont use cellphone for more than 6 min .
The options are to put the phone on speaker mode and hold it at least a foot away from your body or use a headset. They suggested putting up a wire mesh or water curtains, or growing plants to prevent radiation from cell, TV or FM towers in the vicinity of 500 metres to one km.  Radiation from cell phones and towers posed serious health risks, including loss of memory, lack of concentration, disturbances in your digestive system and sleep disorders.


IIT-Bombay professor Girish Kumar warned against cell phone usage for more than six minutes a day as handsets have a specific absorption rate (capacity to absorb radiation) of 1.6 watts per kg and thus can absorb radiation only for six minutes a dayand later can harm the body. "After formally speaking on the cell phone, one should switch to a landline phone," he added, pointing out that the brain had a high risk of getting affected by radiation.

He said the antennas of repeaters near residential areas or working stations should not give a radiation frequency of more than 0.1 watts. Similarly, Kumar said, the ideal wattage for cell towers should be two watts in densely populated urban areas.

"Towers give off radiation of up to 400 watts as more carriers are fitted on the antennas. A microwave is of 500-watt capacity so imagine the effect towers can leave on your body," he added. According to Kumar, wi-fi, of not more than 100 mw, should also be switched off when not in use.

Anatomy and Function of the brain

Learning Head CT
Learning Brain MRI

Parital Lobe stroke

Blood supply to Brain

Hypertension affects deep branches of cerebral artery----> causes Lacunar infarct------> affect Basal Ganglia, Internal Capsule (paralysis), Subthalamus(Hemiballismus)..

Hypotension affects watershed area causing watershed Infarct. area lies between ACA and MCA on lateral aspect of cerebral hemisphere.  Affect pre and Post central gyrus----affect trunk area 'Men in barrel syndrome'  means UL---normal function, LL-Normal function but Trunk is affectted both sensory and motor part.

MCA: Supplies contralateral UL, Neck and face, both sensory and motor part.

ACA: Supplies contralateral Pelvis and LL, both sensory and Motor part.

PCA: Supplies Occipital Lobe

So occlusion of 

MCA: Contralateral spastic paresis and anesthesia of UL, Neck and Face.

ACA: Contralateral spastic paresis and anesthesia of LL and Pelvis.

PCA: Contralateral homonymous Hemianopia with macular sparing.

Other findings:

Left MCA: 

• aphasia- broca's, Wernicke, Conduction.
• Angular Gyrus: Gesterman Syndrome

Right MCA:

• Inferior parietal Lobule: Unilateral neglect of Left side of body

Lacunar Stroke VS Major Cerebral Artery Stroke:

Lacunar stroke affects all UL, LL and face altogether while Major cerebral Artery affect different aprt of the body like UL, face   vs   LL.  

Internal Capsule Infarct:

It has Ant limb, genu and Posterior limb.

Ant Limb: contains Talamo-mammilary tr---not significant sign and symptoms

genu: contains coricobulbar tr ----- affects entire Lower Face.

Post Limb: contains all 3 major tracts: CST, Talamocortical Tr and Spinothalamic tr --- cause contralateral spastic paralysis, contralateral loss of touch, pain and temerature sensation.

Here are Some really good images showing blood supply to different part of the brain....







Brain stem arteries - anterior view 

1. Posterior cerebral artery
2. Superior cerebellar artery
3. Pontine branches of the basilar artery
4. Anterior inferior cerebellar artery
5. Internal auditory artery
6. Vertebral artery
7. Posterior inferior cerebellar artery
8. Anterior spinal artery
9. Basilar artery

MCA stroke

Decreased Flow right MCA

Lateral Medullary Syndrome/ Wallenberg syndrome

Brain stem arteries - anterior view 

1. Posterior cerebral artery
2. Superior cerebellar artery
3. Pontine branches of the basilar artery
4. Anterior inferior cerebellar artery
5. Internal auditory artery
6. Vertebral artery
7. Posterior inferior cerebellar artery
8. Anterior spinal artery
9. Basilar artery

Case : Cerebral Angiogram, 2/3/93: Left Vertebral Artery Dissection
CC: Falling to left.

Hx: 26y/oRHF fell and struck her head on the ice 3.5weeks prior to presentation. There was no associated loss of consciousness. She noted a dull headache and severe sharp pain behind her left ear 8 days ago. The pain lasted 1-2 minutes in duration. The next morning she experienced difficulty walking and consistently fell to the left. In addition the left side of her face had become numb and she began choking on food. Family noted her pupils had become unequal in size. She was seen locally and felt to be depressed and admitted to a psychiatric facility. She was subsequently transferred to hospital following evaluation by a local ophthalmologist.

MEDS: Prozac and Ativan(both recently started at the psychiatric facility).
PMH: 1)Right esotropia and hyperopia since age 1year. 2)recurrent UTI.
FHx: Unremarkable.
SHx: Divorced. Lives with children. No spontaneous abortions. Denied ETOH/Tobacco/Illicit Drug use.

EXAM: BP138/110 HR85 RR16 37.2C
MS: A&O to person, place, time. Speech fluent and without dysarthria. Intact naming, comprehension, repetition.
CN: Pupils 4/2 decreasing to 3/1 on exposure to light. Optic Disks flat. VFFTC. Esotropia OD, otherwise EOM full. Horizontal nystagmus on leftward gaze. Decreased corneal reflex, OS. Decreased PP/TEMP sensation on left side of face. Light touch testing normal. Decreased gag response on left. Uvula deviates to right. The rest of the CN exam was unremarkable.
Motor: 5/5 strength throughout with normal muscle bulk and tone.
Sensory: Decreased PP and TEMP on right side of body. PROP/VIB intact.
Coord: Difficulty with FNF/HKS/RAM on left. Normal on right side.
Station: No pronator drift. Romberg test not noted.
Gait: unsteady with tendency to fall to left.
Reflexes: 3/3 throughout BUE and Patellae. 2+/2+ Achilles. Plantar responses were flexor, bilaterally.
Gen Exam: Obese. In no acute distress. Otherwise unremarkable.
HEENT: No carotid/vertebral/cranial bruits.

COURSE: PT/PTT, GS, CBC, TSH, FT4 and Cholesterol screen were all within normal limits. HCT on admission was negative. MRI Brain (done locally 2/2/93) was reviewed and a left lateral medullary stroke was appreciated. The patient underwent a cerebral angiogram on 2/3/93 which revealed significant narrowing of the left vertebral artery beginning at C2 and extending to and involving the basilar artery. There is severe, irregular narrowing of the horizontal portion above the posterior arch of C1. The findings were felt consistent with a left vertebral artery dissection. Neuro-opthalmology confirmed a left Horner's pupil by clinical exam and history. Cookie swallow study was unremarkable. The Patient was placed on Heparin then converted to Coumadin. The PT on discharge was 17.
She remained on Coumadin for 3 months and then was switched to ASA for 1 year. An Otolaryngologic evaluation on 10/96 noted true left vocal cord paralysis with full glottic closure. A prosthesis was made and no surgical invention was done.




Discussion:

Wallenberg’s syndrome (WS) is usually caused by infarction of the lateral portion of the medulla, more often caused by vertebral artery (VA) disease. In classical WS, pain and temperature sensation loss on the face is ipsilateral to the lesion in the medulla. However, contralateral and bilateral sensory abnormalities may also occur.

In neuroanatomical descriptions of the brain stem, the descending spinal nucleus/tract (DSN/T) and the ventral ascending tract of the trigeminal nerve or ventral trigeminothalamic tract (VTT) are located in the posterolateral medulla. The VTT is positioned adjacent to the medial lemniscus or medial to the lateral spinothalamic tract (LST) in the dorsomedial corner of the inferior olive . DSN/T lesions are associated with decrease in pain and temperature sensation on the ipsilateral face, while injuries to the VTT crossing fibers produce diminished sensation on the contralateral face. Thus, it would be expected that infarcts extending medially and anteriorly in the dorsolateral medulla would cause pain and temperature sensory loss on the contralateral face, opposite to the side of the lesion.

Some studies reported lateral medullary infarcts (LMIs) to be more medially located in patients with contralateral facial pain/temperature sensory loss than in those with ipsilateral facial sensory abnormalities but others did not confirm these findings. 

Bilateral Thalamic Stroke

Case : MRI brain: Top of the Basilar/bilateral thalamic strokes.
CC: Sudden onset blindness.

Hx: This 58 y/o RHF was in her usual healthy state, until 4:00PM, 1/8/93, when she suddenly became blind. Tongue numbness and slurred speech occurred simultaneously with the loss of vision. The vision transiently improved to "severe blurring" enroute to a local ER, but worsened again once there. While being evaluated she became unresponsive, even to deep noxious stimuli. She was transferred to UIHC for further evaluation. Upon arrival at UIHC her signs and symptoms were present but markedly improved.

PMH: 1)hysterectomy many years previous. 2) herniorrhaphy in past. 3)DJD, relieved with NSAIDs.
FHx/SHx: Married x 27yrs. Husband denied Tobacco/ETOH/illicit drug use for her.
Unremarkable FHx.
MEDS: none.

EXAM: Vitals: 36.9C HR93 BP 151/93 RR22 98%O2Sat
MS: somnolent, but arousable to verbal stimulation. minimal speech. followed simple commands on occasion.
CN: Blinked to threat from all directions. EOM appeared full, Pupils 2/2 decreasing to 1/1. +/+Corneas. Winced to PP in all areas of Face. +/+Gag. Tongue midline. Oculocephalic reflex intact.
Motor: UE 4/5 proximally. Full strength in all other areas. Normal tone and muscle bulk.
Sensory: Withdrew to PP in all extremities.
Coord/Gait: ND.
Reflexes: 2+/2+ throughout UE, 3/3 patella, 2/2 ankles, Plantar responses were flexor bilaterally.
Gen exam: unremarkable.

Course: MRI Brain revealed bilateral thalamic strokes. Transthoracic echocardiogram (TTE) showed an intraatrial septal aneurysm with right to left shunt. Transesophageal echocardiogram(TEE) revealed the same. No intracardiac thrombus was found. Lower extremity dopplers were unremarkable. Carotid duplex revealed 0-15% bilateral ICA stenosis. Neuroophthalmologic evaluation revealed evidence of a supranuclear vertical gaze palsy OU (diminished up and down gaze). Neuropsychologic assessment 1/12-15/93 revealed severe impairment of anterograde verbal and visual memory, including acquisition and delayed recall and recognition. Speech was effortful and hypophonic with very defective verbal associative fluency. Reading comprehension was somewhat preserved, though she complained that despite the ability to see type clearly, she could not make sense of words. There was impairment of 2-D constructional praxis. A follow-up Neuropsychology evaluation in 7/93 revealed little improvement. Laboratory studies, TSH, FT4, CRP, ESR, GS, PT/PTT were unremarkable. Total serum cholesterol 195, Triglycerides 57, HDL 43, LDL 141. She was placed on ASA and discharged1/19/93.
She was last seen on 5/2/95 and was speaking fluently and lucidly. She continued to have mild decreased vertical eye movements. Coordination and strength testing were fairly unremarkable. She continues to take ASA 325mg qd.

Stroke seen on contrast CT only

Case : Brain CT with contrast, 1/19/93: Abnormal Gyriform enhancing lesion(stroke) in the left parietal region, not seen on non-contrast HCTs on 1/8/93 and 1/14/93.
CC: Confusion.

Hx: 71 y/o RHM ,with a history of two strokes( one in 11/90 and one in 11/91), had been in a stable state of health until 12/31/92 when he became confused, and displayed left-sided weakness and difficulty speaking. The symptoms resolved within hours and recurred the following day. He was then evaluated locally and HCT revealed an old right parietal stroke. Carotid duplex scan revealed a "high grade stenosis" of the RICA. Cerebral Angiogram revealed 90%RICA and 50%LICA stenosis. He was then transferred to UIHC Vascular Surgery for carotid endarterectomy. His confusion persisted and he was evaluated by Neurology on 1/8/93 and transferred to Neurology on 1/11/93.

PMH: 1)cholecystectomy. 2)inguinal herniorrhaphies, bilaterally. 3)ETOH abuse: 3-10 beers/day. 4)Right parietal stroke 10/87 with residual left hemiparesis (Leg worse than arm). 5) 2nd stoke in distant past of unspecified type.
MEDS: None on admission.
FHx: Alzheimer's disease and stroke on paternal side of family.
SHx: 50+pack-yr cigarette use.
ROS: no weight loss. poor appetite/selective eater.
EXAM: BP137/70 HR81 RR13 O2Sat 95% Afebrile.
MS: Oriented to city and month, but did not know date or hospital. Naming and verbal comprehension were intact. He could tell which direction Iowa City and Des Moines were from Clinton and remembered 2-3 objects in two minutes, but both with assistance only. Incorrectly spelled "world" backward, as "dlow."
CN: unremarkable except neglects left visual field to double simultaneous stimulation.
Motor: Deltoids 4+/4-, biceps 5-/4, triceps 5/4+, grip 4+/4+, HF4+/4-, HE 4+/4+, Hamstrings 5-/5-, AE 5-/5-, AF 5-/5-.
Sensory: intact PP/LT/Vib.
Coord: dysdiadochokinesis on RAM, bilaterally.
Station: dyssynergic RUE on FNF movement.
Gait: ND
Reflexes: 2+/2+ throughout BUE and at patellae. Absent at ankles. Right plantar was flexor; and Left plantar was equivocal.

COURSE: CBC revealed normal Hgb, Hct, Plt and WBC, but Mean corpuscular volume was large at 103FL(normal 82-98). Urinalysis revealed 20+WBC. GS, TSH, FT4, VDRL, ANA and RF were unremarkable. He was treated for a UTI with amoxacillin. Vitamin B12 level was reduced at 139pg/ml (normal 232-1137). Schillings test was inconclusive dure to inability to complete a 24hour urine collection. He was placed on empiric Vitamin B12 1000mcg IM qd x 7 days; then qMonth. He was also placed on Thiamine 100mg qd, Folate 1mg qd, and ASA 325mg qd. His ESR and CRP were elevated on admission, but fell as his UTI was treated.
EEG showed diffuse slowing and focal slowing in the theta-delta range in the right temporal area. HCT with contrast on 1/19/93 revealed a gyriform enhancing lesion in the left parietal lobe consistent with a new infarct; and an old right parietal hypodensity(infarct). His confusion was ascribed to the UTI in the face of old and new strokes and Vitamin B12 deficiency. He was lost to follow-up and did not undergo carotid endarterectomy.




http://www.uiowa.edu/~c064s01/nr085.htm