Stroke in children
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Stroke is an emergency condition caused by a blocked artery or burst blood vessel in the brain. It can lead to serious disability or death if brain cells are not quickly treated. The main types of stroke are ischemic, caused by a blockage, and hemorrhagic, caused by a burst blood vessel. Timely treatment is critical to minimize brain cell death and damage. Management involves stabilizing vital functions, rapidly diagnosing the type of stroke, and administering appropriate treatments such as clot-busting drugs to reduce disability. A multidisciplinary approach is needed for long-term care and rehabilitation.
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Stroke in children
- 4. Stroke is an emergency and a leading c/of death; a BV in brain has a blockage (90%) or bursts (adults). No Rx.: brain cells quickly die: serious disability/death 90%
- 5. Stroke is sudden onset of focal neuro-deficit due to occlusion of blood supply or hemorrhage in the brain causing SS lasting >24h SS: symptoms and signs. BE: both eyes Definition
- 6. Bangladesh Scenario • Stroke is the 3rd leading c/of death • WHO: Bangladesh at mortality from stroke ranks 84 • Prevalence: 0.3%. HTN is the main cause of IS and HS • Disability-Adjusted Life-Years from stroke: 485/10k • GoB needs to emphasize healthcare development to cope with stroke
- 8. • Hemorrhagic strokes – 11.4% • Ischemic strokes – 88.6% Prothrombotic states – 38.7% Cardiac disease – 19.3% Hyperlipidemia – 16.0% Homocysteinuria – 14.6% 99 Adult Pts. at AIIMS, New Delhi
- 9. Typical SS: Sudden numbness/weakness, esp. on 1 side, sudden vision changes in 1/BE, dysphagia; sudden: severe HA, dizziness, confusion, problem walking, balance, speaking/understanding
- 10. Test: F.A.S.T.: Face: smile: 1 side droops? Raise Arms: does 1 side drift down? Speech. Can s/he repeat a simple sentence? Trouble talking, slur words? Time
- 12. • Not exactly known; 3-13/100k/y • In INDIA: 13-33/100k/y • USA: 2.52/100k/y –14y – 1.89– hemorrhagic – 0.65- ischemic • Children & Young adults: <5% of all strokes • Occurs in all age groups (NB-teenagers) • It may even occur before birth • 1/2,300 – 5k/NB have a stroke NB: newborn. LB: live born Incidence in Children
- 13. • Stroke is the 6th c/of death in children while in adult it is 3rd, ranking behind HD & cancer • As common as brain tumors • Impacts of strokes – Mortality 6-40% (hemorrhagic: x2) – Morbidity • Neurological d – 60% • Seizures – 15% • HA
- 14. Risk Factors Childhood Stroke (USA) • Cardiac D 19% • Coagulation D 14% • Dehydration 11% • Vasculitis 7% • Infection 6% • Dissection 5% • Neoplasm 4% • Metabolic D 3% • Moyamoya, SCD, Perinatal Complication, and Others: each 2% Multiple risk factors are often present & predict worse outcome
- 15. Congenital Aortic Stenosis, MS VSD, PDA Cyanotic CHD involving R-L shunt Inherited con. tissue d: Marfan, Ehlers-Danlos syn Acquired Endocarditis, cardiomyopathy Arrthymia, Rh F Psoriatic HD Cardiac Causes Diagonal earlobe crease
- 16. • Disorder of RBC: SCD, Polycythemia • D. of WBC: Leukemia, lymphoma • D. of Platelets: Thrombocytosis, -penia • D. of clotting: Protein C, S deficiency Factor V, antithrombin III deficiency Paroxysmal noc. Hb.nuria IBD, lupus anticoagulants Neonatal & childhood CSVT Hematological Causes
- 17. SCD – 25 % develop stroke by 45y. Recurrent in 67% – IS predominantly in childhood – Hemorrhagic with steroid and HTN – Sinovenous thrombosis, posterior leukoencephalopathy, watershed ischemia – Silent infarcts; more in the frontal lobe (17% under14) – HS (ICH/SAH) in adults – High WBC in inf. and anemia can precipitate IS: ischaemic stroke. HS: hemorrhagic stroke
- 18. Moya –Moya AV malformations Aneurysm Sturge Weber syn Fibromuscular dysplasia VASCULAR DISEASE Normal lateral projection angiogram with injection of IC artery Suzuki grades I to II with narrowing of IC artery before dev. of extensive collateral vessels
- 20. • Infection Meningitis HIV encephalopathy Local head & neck inf. • Autoimmune d. SLE, Takayasu arteritis, PA nodosa Sarcoidosis Mixed CT D INFLAMMATORY DISORDERS
- 21. METABOLIC DISORDERS • Homocystinuria • Pseudoxanthoma elasticum • Fabry disease • Mitochondrial encephalopathies: MELAS Leigh syn Drug induced Amphetamines, cocaine
- 22. • Trauma • Child abuses • Placental embolism • ECMO therapy • Post varicella Misc. Causes
- 26. Thrombosis occludes anterior, middle, posterior basilar, vertebral & internal carotid arteries. Arterial thrombosis more common at atheromatous plaques or stenosis of arteries Thrombi embolise to distal region Causing intracranial ischemia & infarction Intracranial Thrombosis
- 27. Emboli arise mainly from atheromata within great vessel or from heart Intracranial Embolism
- 28. Pathophysiology of Hemorrhage 20 % strokes are from rupture of IC aneurysm Chacot – Bouchard aneurysms are usually due to chr. HTN They usually involve small penetrating (0.8-1.0 mm) lenticulostriate br. of MCA in the basal ganglia, brainstem and midbrain. Cause IC hge.
- 32. Arterial ischemic stroke (AIS) Cerebral SinoVenous thrombosis (CSVT) IC hemorrhage Types of Stroke Syn.
- 33. SIGNS & SYMPTOMS
- 34. Newborns and Infants CN: cranial nerve. HA: headache. V: vomiting
- 35. Weakness/numbness of face, arm/leg, usually on 1 side Trouble walking (weakness/trouble moving 1 side, or incoordination) Problem speaking/understanding: slurred speech, or difficulty in understanding simple directions Severe HA especially with V and sleepiness Children and Teenagers
- 36. Trouble seeing clearly in 1 or both eyes Severe dizziness/incoordination: losing balance/falling New seizures, especially if affecting 1 side of body and followed by paralysis on the side of the seizure activity Progressively worsening non-stop HA with drowsiness and repetitive V, lasting days without relief Complaint of acute onset of the "worst HA of my life" Contd….
- 37. Lesion can be divided in 2 groups based of CN palsy as : CN palsy on same side as that of hemiplegia CN palsy on opposite to that of hemiplegia Localization of Lesion in Hemiplegia
- 38. • Lesion above the level of brain stem (Ipsilateral hemiplegia); at the level of either Cortex Sub cortical region Internal capsule CN Palsy on Same Side as that of H..
- 40. Lobes of the Cerebrum Parietal Lobe Temporal Lobe Frontal Lobe Limbic Lobe Occipital Lobe
- 42. • Hemiparesis or Monoparesis • Involvement: Upper limb > LL or vice versa • Altered sensorium, convulsion • Cortical sensory loss: asteriognosis, agraphesthesia • Aphasia (If dominant cortex) Cortical Lesion
- 43. Frontal Lobe is responsible for higher cognitive functions: • Problem solving • Spontaneity • Memory • Language • Motivation • Judgment • Impulse control • Social/sexual behavior
- 44. • Altered behavior • Upper limb> LL • Motor aphasia • Convulsions • Bladder & bowel involvement • Persistent neonatal reflexes on opposite side Frontal Lobe Involvement
- 45. Parietal Lobe a role in our sensations of touch, smell, taste. It also processes sensory and spatial awareness, and is a key component in eye-hand co-ordination and arm movement It also contains a specialized area called Wernicke area that is responsible for matching written words with the sound of spoken speech
- 46. –Cortical sensory loss –Astereognosis Parietal Lobe Involvement
- 47. Temporal Lobe plays a role in emotions, and is also responsible for smelling, tasting, perception, memory, music, aggressiveness, sexual behavior It also contains the language area
- 48. • TL epilepsy • Sensory aphasia • Memory loss Temporal Lobe Involvement
- 49. Occipital Lobe controls vision and recognition
- 50. OCCIPITAL LOBE INVOLVEMENT Homonymous hemianopia
- 51. INTERNAL CAPSULE LESION Dense hemiplegia Hemianaesthesia Homonymous hemianopia Dysarthria
- 52. SUB CORTICAL LESION Similar to cortical lesion except loss of cortical sensation & convulsions
- 53. • Lesion at/below the level of brain stem (Contra lateral hemiplegia). Lesion can be either of Midbrain Pons Medulla Spinal cord ( b/w C 1 – C4 ) CN Palsy on Opposite Side to that of …
- 54. • Weber Syn.: CN3 palsy + contra lateral hemiplegia • Benedict Syn.: CN3 palsy + contra lateral H + red nucleus affection( tremor, rigidity & ataxia on opposite side) H: hemiplegia Mid brain lesion
- 55. The Pons The pons lies between the midbrain and medulla. Pons means “bridge” Pons connects cerebellum to the rest of the brain and modify the respiratory output of medulla The pons is the origin of several CNs
- 56. • Millard Gubbler Syn.: CN7 palsy + contra lateral H • Foville Syn.: CN6&7 palsy+ contra lateral hemiplegia Pons lesion
- 57. • Jackson Syn.: CN12 palsy + contra lateral hemiplegia Medullary lesion
- 58. • Brown Sequard Syn.: Hemiplegia + CN palsy + differential sensory loss (loss of vibration & joint sense on same side & pain ,touch & temp. on opposite Spinal Cord Lesion
- 59. Focal cerebral ischemia IC hemorrhage Cerebral abscess, encephalitis (HSV) Brain tumor Alternating hemiplegia of infancy MS Malingering/conversion disorder Epilepsy: Todd's paralysis or a focal inhibitory seizure Complicated migraine Differential Diagnosis
- 60. Seizures Raised IC tension Hypertension Aphasia Skeletal deformities Complications
- 61. • FIRST LINE: Performed within 48h of admission • SECOND LINE: Performed within first week • THRID LINE: Performed as per need Diagnostic Evaluation
- 62. CBC Film Blood sugar, BUN, S electrolytes ( Na, K, Ca, Mg, Phos.) AST, ALT, S. lipid profile CXR, CT brain, MRI brain & MR angiography Ultrasonography ANA ECG FIRST LINE
- 65. CT: rapid disappearance of IC hge. from R b. ganglia
- 66. Echo- (transthoracic) with saline contrast Transcranial and/or carotid dopplers MR angiogram, EEG Rh. Factor, S. amino a., urine for organic a. Blood culture. Hb. electrophoresis Complement profile, VDRL Lactate/pyruvate, ammonia CSF: cell count, protein, glucose, lactate SECOND LINE
- 67. Antithrombin III Protein C (activity and antigen) Factor V Leiden mutation Antiphospholipid antibody; Lupus-anticoagulant Anticardiolipin Hypercoagulable Evaluation
- 68. HIV Lyme, Mycoplasma, Cat-scratch titers Cardiac MRI Echocardiogram (transesophageal) Muscle Biopsy DNA testing for MELAS Cerebral angiogram (transfemoral) Leptomeningeal biopsy Serum homocysteine after methionine load THIRD LINE
- 69. MANAGEMENT
- 70. Time = Brain Damage: every second counts. Hypoxia kills brain cells within mins. Clot- busting drugs can curb damage, if used in 3h of attack. Stroke is a top c/of long-term disability
- 71. • 1st step is to DD ischemic & HS • Anticoagulant Rx is contraindicated in HS • Hyperglycemia & HTN worsen the stroke • Multidisciplinary approach General Consideration before Rx
- 72. Rx primarily is directed towards stabilizing systemic factors & management of the underlying causes Arterial Ischemic Stroke (AIS)
- 73. Intracranial tension: 1. Fluid restriction 2. Mannitol 3. Steroids 4. Shunt surgery ( In special case) Hypertension: by appropriate antihypertensive Supportive Care
- 74. Fluid balance Hyperglycemia Hyperthermia Seizures with AED ABT to prevent secondary inf. AED: antiepileptic drugs, ABT: antibiotic Contd…..
- 75. HEPARIN: - • 28U/kg/h in infants, • 20U/kg/h in >1y • 18U/kg/h in older children for 5- 10d • LMW Heparin: 0.5-1U/ml Loading dose 75- 100 /kg iv over 10 min followed by maintenance dose : Antithrombotic Rx
- 76. Antiplatelet: -Aspirin 3-5mg/kg/d Clopidrogel Oral anticoagulants: Wafarin for secondary prevention of stroke if aspirin Fails. Congenital or acquired HD, severe coagulable states, arterial dissection & recurrent AIS or TIA while on aspirin Thrombolytic agents: streptokinase & urokinase to dissolve the existing thrombus Contd….
- 78. Surgical repair of Fallot T Regular phlebotomy for thrombosis in Polycythemia BT to prevent future episodes of stroke in SCD Surgery for AVM & aneurysm Steroids & immunosuppressants in autoimmune d. Specific Rx
- 79. Variable. Mostly dependent upon underlying cause 80% survived 10y after an IS, most with residual hemiparesis Poor prognosis with seizures during infancy, and with an angiographic pattern of Moyamoya disease HS have higher mortality than IS Pts. with HS & coma have higher mortality Prognosis
- 80. Risk Factors for Poor Outcome
- 81. Early Dx and intervention for children with stroke in order to improve their recovery rate and prevent recurrence Early Dx and close monitoring of children at high risk for stroke Education and support for families of children with strokes Education about childhood stroke for HCP Education for the general public about childhood strokes Ongoing research into the causes of childhood stroke and effective Rx and prevention strategies GOAL
Editor's Notes
- Ehlers-Danlos syn.: a group of inherited d that affect con. tissues — primarily your skin, joints and BV walls. Con. tissue is a complex mixture of proteins and other substances that provides strength and elasticity to the underlying structures. EDS usually has overly flexible joints and stretchy, fragile skin. This is a problem if you have a wound that requires stitches, as the skin often isn't strong enough to hold them. A more severe form, called vascular EDS, can cause the walls BV, intestines or uterus to rupture Marfan syn. is an inherited d that affects con. tissue — the fibers that support and anchor your organs and other structures in your body. It most commonly affects the heart, eyes, BV and skeleton. The pt. is usually tall and thin with disproportionately long arms, legs, fingers and toes. The damage can be mild or severe. If your heart or BV are affected, it becomes life-threatening. Rx: medications to keep your BP low to reduce the strain on weakened BV wall. Depending on severity and the part affected, surgery may be necessary Psoriatic HD: HD is more frequent in psoriasis: X3 HD. Severe psoriasis: 54% more likely to have a stroke, 21% heart attack, 53% more likely to die over 10-y. This may be due to inflam. causing atherosclerosis. Increased CRP, in psoriasis and CVD, and pro-inflammatory cytokines secreted by activated T-cells that drive rapid epidermal turnover in psoriatic plaques may also induce the formation of atherosclerotic plaques Diagonal ear lobe crease strongly correlated with CAD in both M and F. However, it correlated with sudden cardiac death only in men. Other risk factors like age and BMI for M and F and hair in the ears and baldness in males
- Protein C is a VK-dependent glycoprotein made in liver. It is activated by thrombin-thrombomodulin on endoth. cells. Activated PC degrades the activated clotting factors Va and VIIIa. Its actions are enhanced by the cofactor, protein S. Protein C also has anti-inflam. and cytoprotective properties Protein S is a VK-dependent anticoagulant protein. The mechanism is unclear, but it has a central role in control of coagulation. Deficiency predisposes to recurrent venous thromboembolism and fetal loss. It is a co-factor for Protein C. Deficiency is associated with an increased risk of thrombosis
- Stroke in SCD It was thought that strokes in SCD were c/by sickle-shaped RBC clumping up and blocking smaller BV. But, larger brain arteries are primary site of strokes in SCD. Because the sickled rbc are rigid, they tend to clump up along the walls of these larger arteries, damaging vessel walls and exposing tissue that gathers more sickle cells and further narrows. Children who have a stroke in the past have a high risk of having another stroke. SCD children have a 67% risk of rec. strokes in 9 mo. It is believed to be a rise in wbc count in a drop in Hb after the first stroke. “Silent” Strokes in SCD can also cause significant morbidity; occur without obvious outward SS. They can be detected only by imaging. 17% SCD children under 14 have silent strokes and the rate increases to 23% by 18, with the size and number of lesions increasing. Silent strokes often occur in frontal areas (responsible for executive abilities: mostly academic achievement and memory): impair intellect, academic ability, attention, visual-spatial skills, language, long-term memory. Early detection through screening and brain imaging is of the utmost importance, since imaging can help prevent recurrences. The strongest predictor of stroke in children with SCD is a previous stroke. Predicting SS that often precede a stroke: A h/of seizures, a previous TIA, New or increased frequency of pain syn. like ac. chest syn (ACS), NS inf, trauma, HTN, low Hb, an abnormal transcranial doppler, increased wbc, increased cerebral BF pressure, a h/of snoring and/or confirmation of sleep apnea
- Moyamoya d is a rare BV d. in which Circle of Willis and the distal segments of the arteries supplying the brain progressively narrow: BF become reduced. It may cause a TIA, stroke or other SS. It mainly affects children, but adults may have it as well: usually in Japan and Asian countries, but people in N America, Europe and other areas also have it SS: Hemiparesis, Monoparesis, Sensory impairment, Involuntary movements, HA, Dizziness or Seizures, MR or Persistent neurologic deficits AVM: a tangle of BV in the brain or on its surface bypasses normal brain tissue and directly diverts blood from the arteries to the veins. Why do brain AVMs occur? We don’t know. Brain AVMs are usually congenital, usually not hereditary Where do brain AVMs occur? Anywhere. Do brain AVMs change or grow? Most don’t grow or change, although may dilate. Some may shrink due to clots. Some may enlarge to redirect blood in adjacent vessels toward an AVM. What are the symptoms of a brain AVM? vary depending on site: >50% have an ICH. 20% have focal or generalized seizures. Patients may have localized pain in the head due to increased BF. 15% may have difficulty with movement, speech and vision. What causes brain AVMs to bleed? A brain AVM contains abnormal and, therefore, “weakened” blood vessels that direct blood away from normal brain tissue. These abnormal and weak blood vessels dilate over time. Eventually they may burst from the high pressure of blood flow from the arteries, causing bleeding into the brain. What are the chances of a brain AVM bleeding? The chance of a brain AVM bleeding is 1 percent to 3 percent per year. Over 15 years, the total chance of an AVM bleeding into the brain — causing brain damage and stroke — is 25 percent. Does 1 bleed increase the chance of a 2nd bleed? The risk of recurrent IC bleeding is slightly higher for a short time after the first bleed. The risk during the first y after initial bleeding was 6% and then dropped to the baseline rate. In another study, the risk of recurrence during the first year was 17.9%. The risk of recurrent bleeding may be even higher in the first year after the second bleed and has been reported to be 25 percent during that year. People who are between 11 to 35 years old and who have an AVM are at a slightly higher risk of bleeding Sturge-Weber Syn. or encephelotrigeminal angiomatosis is a cong., non-familial d. of unknown incidence and cause. It is characterized by a cong. facial birthmark and neurological abnormalities. Other SS in SWS: eye and internal organ irregularities. Each case is unique and exhibits the characterizing findings to varying degrees. Neurological Abnormalities in SWS: relate to the dev. of excessive BV on brain surface (angiomas). These are located typically on the occipital region on the same side as the portwine birthmark. These angiomas affect brain function in the region. Seizure is the commonest early problem, often starting by 1y age. The convulsions usually appear on the opposite side of the Port wine Stain and vary in severity. Vigorous attempts are made to control the seizures with medication. Hemiparesis, may develop opposite to the port wine stain. Dev. delay of motor and cognitive skills may also occur to varying degrees
- What is sarcoidosis? Sarcoidosis is an inflam. d. that affects one or more organs but most commonly lungs and LN. As a result of the inflam., abnormal lumps/nodules (granulomas) form in one or more organs. These granulomas may change the normal structure and possibly the function of the affected organ(s). How sarcoidosis progresses: At the tissue or cellular level, sarcoidosis can be divided into 3 phases: The first is inflam. In the 2nd phase, granulomas form. Granulomas are masses/nodules of chr inflamed tissue and are the classic sign. Granulomas are the body’s attempt to wall off or isolate organisms and FB that are difficult for the immune sys to eradicate. In the 3rd phase, fibrosis occurs. If it is extensive in a vital organ, sarcoidosis is sometimes fatal. In some, the disease advances from 1 phase to the next in the tissues of the organ affected. In others, the different phases of tissue changes take place within the same organ at the same time. In many patients with sarcoidosis, the granulomas go away on their own in 2-3y without the patient knowing or doing anything. In others, the granulomas progress to irreversible fibrosis. The immune sys changes that allow one person’s disease to progress while another person’s disease resolves are not well understood and continue to be investigated
- Homocystinuria is an inherited d in which the body is unable to process certain amino a. properly. There are multiple forms of H, which are DD by their SS and genetic cause. The most common form is characterized by myopia, dislocation of the lens, an increased risk of clotting, and osteoporosis or other skeletal abnormalities. Some affected individuals also have developmental delay and learning problems. Less common forms can cause intellectual disability, FTT, seizures, problems with movement, and megaloblastic a. which occurs when a person has a low number of red blood cells (anemia), and the remaining red blood cells are large. SS of H typically develop within the first year of life, although some people with a mild form of the disease may not develop features until later in childhood or adulthood
- Charcot-Bouchard aneurysms are microaneurysms 0.8-1.0mm. They are the principal c/of primary intracerebral hge. and commonly arise at the bifurcation of small arteries that lie deep within the brain parenchyma. They occur at well defined sites, the b. ganglia, pons, cerebellum and subcortical white m. They are associated with chr. HTN and result from infiltration of the arterial walls by lipid and hyaline material - a process referred to as hypertensive lipohyalinosis. Usually involve small penetrating lenticulostriate br. of MCA in the basal ganglia, brainstem and midbrain
- Berry aneurysm: A small aneurysm that looks like a berry and classically occurs at the point at which a cerebral artery departs from circle of Willis. Berry aneurysms frequently rupture and bleed
- Aneurysm in the brain. An aneurysm is a weak area in the wall of a blood vessel that causes the blood vessel to bulge or balloon out. Causes. Aneurysms may be present from birth. Or, it may develop later in life, such as after a Bv is injured. There are many types of brain aneurysms. The most common type is called a berry aneurysm. This type can vary in size from a few mm to over a cm. Giant berry aneurysms can be >2cm. These are more common in adults. Berry aneurysms are passed down through families more often than other types of aneurysms. Other types of cerebral aneurysms involve widening of an entire blood vessel. Or, they may appear as a ballooning out of part of a blood vessel. Such aneurysms can occur in any blood vessel that supplies the brain. Atherosclerosis, trauma, and infection can all injure the blood vessel wall and cause cerebral aneurysms. About 5% of people have a brain aneurysm, but only a small number of these aneurysms cause symptoms or rupture. Risk factors include: Family history of cerebral aneurysms Medical problems such as polycystic kidney disease, coarctation of the aorta, and endocarditis
- Cortical Sensation: Higher-order sensation, or cortical sensation. To test graphesthesia, ask him to close eyes and identify letters or numbers that are being traced onto palm or the tip of finger. To test stereognosis, ask him to close eyes and identify various objects by touch using 1 hand at a time. Test also for tactile extinction on double simultaneous tactile stimulation. Note that graphesthesia, stereognosis, and extinction cannot reliably be tested for unless primary sensation is intact bilaterally. Stereognosis: the faculty of perceiving and understanding the form and nature of objects by the sense of touch; perception by the senses of the solidity of objects Extinction: Somatosensory deficits can be c/by lesions in PN, nerve roots, posterior columns or anterolateral sensory sys. in the SC or brainstem, thalamus, or sensory cortex. Position and vibration sense ascend in the posterior column pathway and cross over in the medulla, while pain and temp. sense cross over shortly after entering SC and then ascend in the anterolateral pathway. Intact primary sensation with deficits in cortical sensation like agraphesthesia or astereognosis suggests a lesion in the contralateral sensory cortex. Note, however, that severe cortical lesions can cause deficits in primary sensation as well. Extinction with intact primary sensation is a form of hemineglect that is most commonly associated with lesions of the R parietal lobe. Extinction can also be seen in R frontal or subcortical lesions, or sometimes in L hemisphere lesions causing mild R hemineglect. The pattern of sensory loss can provide important information that helps localize lesions to particular nerves, nerve roots, and regions of the SC, brainstem, thalamus, cortex
- Primary sensation - asymmetry, sensory level Light touch is best tested with a cotton-swab, but a light finger touch will often suffice, as long as care is taken to make the stimulus fairly reproducible. You can test the relative sharpness of pain by randomly alternating stimuli with the sharp or dull end of a safety pin (new pin for each pt). Temp. sensation can be tested with a cool piece of metal such as a tuning fork. Test vibration sense by placing a vibrating tuning fork on the ball large toe or fingers and asking him to report when the vibration stops. Take care not to place the tuning fork on a bone, since bones conduct the vibration to much more proximal sites, where they can be detected by nerves far from the location being tested Test joint position sense by moving one of his fingers or toes up and down and asking to report which way it moves. Hold the digit lightly by the sides while doing this so that tactile inputs don't provide significant clues to the direction of movement. The digit should be moved very slightly because normal individuals can detect movements that are barely perceptible by eye. 2-point discrimination can be tested with a special pair of calipers, or a bent paper clip, alternating randomly between touching him with 1 or both points. The minimal separation (in mm) at which he can distinguish these stimuli should be recorded in each extremity. As in other parts of the exam, the patient's deficits, as well as the anatomy of the nerves, nerve roots, and central pathways, should be used to guide the exam (see Neuroanatomy through Clinical Cases Chapters 7, 8, and 9). Comparisons should be made from one side of the body to the other and from proximal to distal on each extremity. Note especially if there is a sensory level corresponding to a particular spinal segment below which sensation abruptly changes, since such a change may indicate a spinal cord lesion requiring emergency intervention. Whenever there are uncertainties in the sensory exam, or other parts of the exam, a good strategy is to repeat the relevant portions of the exam several times
- TLE is the commonest partial or localization related E. The overall prognosis for patients with drug resistant medial TLE includes a higher risk for memory and mood difficulties. Usually, the birth, labor, delivery and development of individuals with medial TLE is normal. Medial TLE usually begins at the end of a first or second decade in most cases, following either a seizure with F or an early injury to the brain. What is TLE? The features of seizures beginning in the TL can be extremely varied, but certain patterns are common. There may be a mixture of different feelings, emotions, thoughts, and experiences, which may be familiar or completely foreign. In some cases, a series of old memories resurfaces. In others, the person may feel as if everything—including home and family—appears strange. Hallucinations of voices, music, people, smells, tastes may occur. These features are called “auras” or “warnings.” They may last for just a few seconds, or may continue as long as a minute or two. Experiences during TL seizures vary in intensity and quality. Sometimes the seizures are so mild that the person barely notices. In other cases, the person may be consumed with fright, intellectual fascination, or even pleasure. The experiences and sensations that accompany these seizures are often impossible to describe, even for the most eloquent adult. And of course it is even more difficult to get an accurate picture of what people are feeling What are the types of TLE? TLE accounts for 60% of all E. 2 types; 1 involves the medial or internal structures of TL, while the 2nd, called neocortical TLE, involves the outer portion. The commonest version is medial. MTLE often begins within a structure of the brain called the hippocampus or its surrounding structures. It accounts for almost 80% of all temporal lobe seizures. Medial temporal lobe epilepsy is also considered a syndrome, which means that a lot of different conditions can result in medial temporal lobe epilepsy. Individuals who have medial temporal lobe epilepsy have seizures by definition of temporal lobe origin. There are a lot of different older names for the seizures that occur in temporal lobe epilepsy, including, “psychomotor seizures”, “limbic seizures”, and “temporal lobe seizures.” The modern name for these seizures is “complex partial,” if there is loss of awareness or “simple partial” if awareness is retained. While medial temporal lobe epilepsy is a very common form of epilepsy, it is also frequently resistant to medications and associated with a particular finding on an MRI. This finding is called hippocampal sclerosis (sclerosis means hardening) and it makes this a challenge to treat both medically and oftentimes surgical therapy is the best option for these individuals
- Factor V Leiden is a mutation of factor V. This can increase risk of developing abnormal blood clots (thrombophilia), usually in veins. Most cases never develop abnormal clots. However, clots can lead to long-term health problems or become life-threatening. Both men and women can have it, but F may have more clots during preg or when taking estrogen. If you have it and have clots, medications can lessen risk and help you avoid potentially serious complications Lupus anticoagulants: are antibodies against substances in the lining of cells. These substances prevent blood clotting in a test tube. They are called phospholipids. These antibodies may have an abnormally high risk of clotting. Causes: Most often found in SLE. May also occur if: certain medicines, such as phenothiazines, phenytoin, hydralazine, quinine, and the amoxicillin; IBD, infections, certain kinds of tumors; may be idiopathic. Symptoms: may be asymptomatic. Symptoms: Blood clots in the legs or the lungs as well as stroke or heart attack; Recurrent miscarriages Exams and Tests: PTT, Russell viper venom time, Thromboplastin inhibition test Treatment: Often, no need if no symptoms or if no blood clot in the past. Avoid most birth control pills or hormone treatments for menopause (women). Do not smoke or use other tobacco products. Get up and move around during long plane flights or other times when you have to sit or lie down for extended periods. Move your ankles up and down when you can not move around. Your doctor may prescribe blood thinning medicines (such as heparin and warfarin) to help prevent blood clots: After surgery After a bone fracture With active cancer When you need to set or lie down for long periods of time, such as during a hospital stay or recovering at home. You may also need to take blood thinners for 3 to 4 weeks after surgery to lower your risk of blood clots. Outlook (Prognosis) Most of the time, outcome is good with proper treatment. Some people may have blood clots that are hard to control with treatments. Symptoms may recur