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

Recurrent artery of Heubner on left

Case : CT Brain, 1/5/1993: Stroke, recurrent artery of Heubner on left.
CC: Falls

Hx: This 51y/o RHF fell four times on 1/3/93, because her "legs suddenly gave out." She subsequently noticed weakness involving the right leg, and often required the assistance of her arms to move it. During some of these episodes she appeared mildly pale and felt generally weak; her husband would give her 3 teaspoons of sugar and she would appear to improve, thought not completely. During one episode she held her RUE in an "odd fisted posture." She denied any other focal weakness, sensory change, dysarthria, diplopia, dysphagia or alteration of consciousness. She did not seek medical attention despite her weakness. Then, last night, 1/4/93, she fell again ,and because her weakness did not subsequently improve she came to UIHC for evaluation on 1/5/93.

MEDS: Micronase 5mg qd, HCTZ, quit ASA 6 months ago(tired of taking it).
PMH: 1)DM type 2, dx 6 months ago. 2)HTN. 3)DJD. 4)s/p Vitrectomy and retinal traction OU for retinal detachment 7/92. 5) s/p Cholecystemomy,1968. 6) Cataract implant, OU,1992. 7) s/p C-section.
FHx: Grand Aunt(stroke), MG(CAD), Mother(CAD, died MI age 63), Father(with unknown CA), Sisters(HTN), No DM in relatives.
SHx: Married, lives with husband, 4 children alive and well. Denied tobacco/ETOH/illicit drug use.
ROS: intermittent diarrhea for 20 years.
EXAM: BP164/82 HR64 RR18 36.0C
MS: A & O to person, place, time. Speech fluent and without dysarthria. Intact naming, comprehension, reading.
CN: Pupils 4.5(irregular)/4.0(irregular) and virtually fixed. Optic disks flat. EOM intact. VFFTC. Right lower facial weakness. The rest of the CN exam was unremarkable.
Motor: 5/5 BUE with some question of breakaway. LE: HF and HE 4+/5, KF5/5, AF and AE 5/5. Normal muscle bulk and tone.
Sensory: intact PP/VIB/PROP/LT/T/graphesthesia.
Coord: slowed FNF and HKS (worse on right).
Station: no pronator drift or Romberg sign.
Gait: Unsteady wide-based gait. Unable to heel walk on right.
Reflexes: 2/2+ throughout(Slightly more brisk on right). Plantar responses were downgoing bilaterally.
HEENT: N0 Carotid or cranial bruits.
Gen Exam: unremarkable.

COURSE: CBC, GS(including glucose), PT/PTT, EKG, CXR on admission, 1/5/93, were unremarkable. HCT, 1/5/93, revealed a hypodensity in the left caudate consistent with ischemic change. Carotid Duplex: 0-15%RICA, 16-49%LICA; antegrade vertebral artery flow, bilaterally. Transthoracic echocardiogram showed borderline LV hypertrophy and normal LV function. No valvular abnormalities or thrombus were seen.
The patient's history and exam findings of right facial and RLE weakness with sparing of the RUE would invoke a RACA territory stroke with recurrent artery of Heubner involvement causing the facial weakness.


http://www.uiowa.edu/~c064s01/nr079.htm

Pontine stoke Image

Pontine Stroke

Case : MRI Brain, 11/23/92: Right pontine pyramidal tract infarct
CC: Left sided weakness.
Hx: 74 y/o RHF awoke from a nap at 11:00AM on 11/22/92 and felt weak on her left side. She required support on that side to ambulate. In addition, she felt spoke as though she "was drunk." Nevertheless, she was able to comprehend what was being spoken around her. Her difficulty with speech completely resolved by 12:00 noon. She was brought to UIHC ETC at 8:30AM on 11/23/92 for evaluation.
MEDS: none. Allergies: ASA/ PCN both cause rash.
PMH: 1)?HTN. 2)COPD. 3)h/o hepatitis(unknown type). 4)Macular degeneration.
SHx: Widowed; lives alone. Denied ETOH/Tobacco/illicit drug use.
FHx: unremarkable.
EXAM: BP191/89 HR68 RR16 37.2C
MS: A & O to person, place and time. Speech fluent; without dysarthria. Intact naming, comprehension, and repetition.
CN: Central scotoma, OS(old). Mild upper lid ptosis, OD(old per picture). Lower left facial weakness.
Motor: Mild Left hemiparesis (4+ to 5- strength throughout affected side). No mention of muscle tone in chart.
Sensory: unremarkable.
Coord: impaired FNF and HKS movement secondary to weakness.
Station: Left pronator drift. No Romberg sign seen.
Gait: Left hemiparetic gait with decreased LUE swing.
Reflexes: 3/3+ biceps and triceps. 3/3+ patellae. 2/3+ ankles with 3-4beats of non-sustained ankle clonus on left. Plantars: Left babinski sign; and flexor on right.
General Exam: 2/6 SEM at left sternal border.
COURSE: GS, CBC, PT, PTT, CK, ESR were within normal limits. ABC 7.4/46/63 on room air. EKG showed a sinus rhythm with right bundle branch block. MRI brain, 11/23/95, revealed a right pontine pyramidal tract infarction. She was treated with Ticlopidine 250mg bid. On 11/26/92, her left hemiparesis worsened. A HCT, 11/27/92, was unremarkable. The patient was treated with IV Heparin. This was discontinued the following day when her strength returned to that noted on 11/23/95. On 11/27/92, she developed angina and was ruled out for MI by serial EKG and cardiac enzyme studies. Carotid duplex showed 0-15% bilateral ICA stenosis and antegrade vertebral artery flow bilaterally. Transthoracic echocardiogram revealed aortic insufficiency only. Transesophageal echocardiogram revealed trivial mitral and tricuspid regurgitation, aortic valvular fibrosis. There was calcification and possible thrombus seen in the descending aorta. Cardiology did not feel the later was an indication for anticoagulation. She was discharged home on Isordil 20 tid, Metoprolol 25mg q12hours, and Ticlid 250mg bid.

Thalamic Infarct

Case : MRI Brain: subacute right thalamic infarct. CC: Left hemiplegia. Hx: 58 y/o RHF awoke at 1:00AM on 10/23/92 with left hemiplegia and dysarthria which cleared within 15 minutes. She was seen at a local ER and neurological exam and CT Brain were reportedly unremarkable. She was admitted locally. She then had two more similar spells at 3AM and 11AM with resolution of the symptoms within an hour. She was placed on IV Heparin following the 3rd episode and was transferred to UIHC. She had not been taking ASA. PMH: 1)HTN. 2) Psoriasis. SHx: denied ETOH/Tobacco/illicit drug use. FHx: unknown. MEDS: Heparin only. Exam: BP160/90 HR145 (supine). BP105/35 HR128 (light headed, standing) RR12 T37.7C MS: Dysarthria only. Lucid thought process. CN: left lower facial weakness only. Motor: mild left hemiparesis with normal muscle bulk. Mildly increased left sided muscle tone. Sensory: unremarkable. Coordination: impaired secondary to weakness on left. Otherwise unremarkable. Station: left pronator drift. Romberg testing not done. Gait: not tested. Reflexes: symmetric; 2+ throughout. Gen Exam: CV: Tachycardic without murmur. Course: The patients signs and symptoms worsening during and after standing to check orthostatic blood pressures. She was immediately placed in a reverse Trendelenburg position and given IV fluids. Repeat neurologic exam at 5PM on the day of presentation revealed a return to the initial presentation of signs and symptoms. PT/PTT/GS/CBC/ABG were unremarkable. EKG revealed sinus tachycardia with rate dependent junctional changes. CXR unremarkable. MRI Brain was obtained and showed an evolving right thalamic/lentiform nucleus infarction best illustrated by increased signal on the Proton density weighted images. Over the ensuing days of admission she had significant fluctuations of her BP(200mmHG to 140mmHG systolic). Her symptoms worsened with falls in BP. Her BP was initially controlled with esmolol or labetalol. Renal Ultrasound, abdominal/pelvic CT, renal function scan, serum and urine osmolality, urine catecholamines/metanephrine studies were unremarkable. Carotid doppler study revealed 0-15%BICA stenosis and antegrade vertebral artery flow, bilaterally. Transthoracic echocardiogram was unremarkable. Cerebral angiogram was performed to r/o vasculitis. This revealed narrowing of the M1 segment of the right MCA. This was thought secondary to atherosclerosis and not vasculitis. She was discharged on ASA, Procardia XL, and Labetalol.