wed- 8-9 thurs- 11-12 10/13/20101dr. alka stoelinga
TRANSCRIPT
Wed- 8-9Thurs- 11-12
10/13/2010 1Dr. Alka Stoelinga
Focal neurological deficit=Focal neurologic signs also known as focal signs or focal CNS signs are perceptual or behavioral impairments which are caused by lesions in a particular area of the central nervous system.
• Frontal lobe signs usually involve the motor system:– unsteadiness in walking– muscular rigidity, resistance to passive movements of the limbs (hypertonia)– paralysis of a limb (monoparesis) or a larger area on one side of the body
(Hemiparesis)– paralysis face and eye movements– inability to express oneself/ broken speech described as an expressive aphasia
(Broca's aphasia)– focal seizures which can spread to adjacent areas (Jacksonian seizure)– grand mal or tonic-clonic seizures– changes in personality such as disinhibition, rage without provocation; or loss
of initiative and concern, apathy, akinetic mutism, general retardation– "frontal release" signs, i.e. reappearance of primitive reflexes such as the
snout reflex, the grasp reflex, and the palmar-mental reflex– unilateral loss of smell (anosmia)
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• Parietal lobe signs usually involve somatic sensation, and may include:– impairment of tactile sensation– impairment of proprioception, i.e. postural sensation and
sensation of passive movement– sensory and visual neglect syndromes, i.e. inability to pay
attention to things in certain parts of the person's sensory or spatial environment. This can be as extreme as denial of a limb.
– loss of ability to read, write or calculate (dyslexia, dysgraphia, dyscalculia)
– loss of ability to find a defined place (geographical agnosia)
– loss of ability to identify objects based on touch (astereognosia)
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• Temporal lobe signs usually involve auditory sensation and memory, and may include:– deafness without damage to the structures of the ear,
described as cortical deafness– tinnitus, auditory hallucinations– loss of ability to comprehend music or language,
described as a sensory aphasia (Wernicke's aphasia)– amnesia, memory loss (affecting either long- or short-
term memory or both)– other memory disturbances such as déjà vu– complex, multimodal hallucinations– complex partial seizures (temporal lobe epilepsy)
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• Occipital lobe signs– Occipital lobe signs usually involve visual sensation, and
may include:– total loss of vision (cortical blindness)– loss of vision with denial of the loss (Anton's syndrome)– loss of vision on one side of the visual field of both eyes
(homonymous hemianopsia)– visual agnosias, i.e. inability to recognize familiar objects,
colors, or faces– visual illusions such as micropsia (objects appear smaller)
and macropsia (objects appear larger)– visual hallucinations, displaying elementary forms, such as
zigzags and flashes, in one half of the visual field only for each eye. (In contrast, temporal lobe visual hallucinations display complex forms, and fill the entire visual field.)
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• Damage to the Limbic System involves loss or damage to memory, and may include:– Loss or confusion of long-term memory prior to
focal neuropathy (Retrograde amnesia)– Inability to form new memories (Anterograde
amnesia)– Loss of, or reduced emotions (Apathy).– Loss of olfactory functions.– Loss of decision making ability.
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• Cerebellar signs– Cerebellar signs usually involve balance and
coordination, and may include:– unsteady and clumsy motion of the limbs or torso
(ataxia)– inability to coordinate fine motor activities
(intention tremor), e.g. "past-pointing" (pointing beyond the finger in the finger-nose test)
– inability to perform rapid alternating movements (dysdiadochokinesis), e.g. inability to rapidly flip the hands
– involuntary left-right eye movements (nystagmus)
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• Brainstem signs– Brainstem signs can involve a host of specific
sensory and motor abnormalities, depending on which fiber tracts and cranial nerve nuclei are affected.
• Spinal cord signs– Spinal cord signs generally involve unilateral
paralysis with contralateral loss of pain sensation
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• TPA= Tissue plasminogen activator (catalyses conversion of plasminogen into plasminbreaks down clot)
• Afib= Atrial fibrillation• Hge= Hemorrhage• Aura= An aura is a distinct perception, either visual, motor, sensory,
or psychological felt around the time a seizure occurs • Post-ictal= altered state of consciousness that a person enters after
experiencing a seizure. – It usually lasts between 5 and 30 minutes, but sometimes longer in
the case of more severe seizures– Is characterized by drowsiness, confusion, nausea, hypertension,
headache or migraine and other disorienting symptoms.– Additionally, emergence from this period is often accompanied by
amnesia or other memory defects.– It is during this period that the brain recovers from the trauma of the
seizure
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Seizures
• Seizure is a paroxysmal event due to abnormally discharging central nervous system neurons.
• Epilepsy is defined as a group of disorders in which there are recurrent episodes of altered cerebral function associated with paroxysmal excessive and hypersynchronous discharge of cerebral neurons.– It is a condition of recurrent seizures due to a chronic
underlying process.
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SEIZURE LOSS OF CONSCIOUSNESS
AURA + -
CYANOSIS + -
TONGUE BITE + -
POST-ICTAL CONFUSION + -
POST-ICTAL HEADACHE + -
POST-ICTAL AMNESIA + -
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Etiology/ Causes of seizures• Vascular (Stroke, bleed, arteriovenous malformations)• Infection (Meningitis, abscess, encephalitis)• Trauma (Especially penetrating injuries)• Autoimmune (CNS vasculitis)• Metabolic (Hyponatraemia, hypocalcaemia,
hypomagnesaemia, hypoglycemia, hypoxia, drug overdose or withdrawal)
• Idiopathic• Neoplasm• pSychiatric[Pneumonic (Seizures are caused by “VITAMINS”)]
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Causes of seizure according to age group
• 0-2 years– Birth asphyxia– Birth injury– Neonatal sepsis
• 2-12 years– Idiopathic– Head injury– Fever– Infections (Meningitis,
encephalitis)
• 12-35 years– Idiopathic– Head injury– Drugs and toxin- alcohol,
antidepressants, amphetamines– Vascular malformations,
aneurysm, tumors• Above 35 years
– Cerebral tumors– Vascular malformations,
aneurysms, CVA, Vasculitis like SLE– Metabolic: Uremia, hepatic failure,
hypoglycemia– Multiple sclerosis
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Diagnosing a case of epilepsy
1. Detailed history from the patient himself or from an eye witness regarding
2. Any injury- Tongue bite, bruises3. Symptoms of aura and its duration4. Defecation/ micturation/ salivation during the
episode5. Any abnormal movements- limb stiffening, jerky
movements, automatism6. Post ictal symptoms: Limb/ muscular pains,
headache, drowsiness, disorientation,Sleepiness
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Physical examination
Pt may be absolutely normalHowever, examine for1. Head, neck, eyes, tongue for any bruises2. Vitals3. Head- for any trauma4. Skin lesions: Neurofibromas, Epiloia (Tuberous
sclerosis)5. Visual and optic field6. Limbs: Hemiparesis, hyperreflexia
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Clinical presentation
• Sudden onset of paroxysmal, involuntary abnormal movement
• With or without loss of consciousness• With or without aura• Postictal phase- Disorientation, sleepiness muscle
aches• Incontinence• Tongue bite• Headache
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Types of seizuresAccording to the source of the seizure within the brain• Partial or focal onset seizures- Localized
– According to the level of consciousness affected• Simple Partial seizures (Consciousness unaffected)• Complex partial seizures (Consciousness affected)
• Generalized seizures- Distributed– According to the effect on the body
• Absence• Myoclonic• Clonic• Tonic• Tonic-clonic• Atonic
• Mixed– Both partial and generalized seizure in same patient
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Factors precipitating seizure
• Sleep deprivation• Alcohol (Withdrawal)• Recreational drug misuse• Physical and mental exhaustion• Flickering lights, including TV and computer
screens• Intercurrent infections and metabolic disorders• Sometimes: Loud noises
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Management• After diagnosis, explanation regarding its curability should be given to the
patient or their relatives• Immediate care of seizure (Outside hospital)
– Move the patient away from danger (Fire/ water/ machinery)– After the convulsions cease, turn the patient into recovery/ semiprone
position to ensure proper airway– If convulsion continues for more than 5 mins or recurs without person
regaining consciousness, seek immediate medical attention– Padded gag/ rolled handkerchief should NOT be kept in mouth between teeth
to avoid tongue bite– DO NOT leave the patient alone for next 30-60 mins until he regains full
consciousness (Drowsy/ confused) – Oxygen at high concentration, if available, to prevent cerebral hypoxia
• Restrict patient to:– Work near fire/ water and machineries– Driving, cycling, swimming, mountaineering
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Investigations• Electroencephalogram (EEG)• CBC, ESR, Electrolytes, blood urea, calcium• Glucose• Arterial blood gases• Liver function tests (LFT)• Toxicology scanning• Serological tests for syphilis• HIV- for high risk groups• ECG/CT/ MRI
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Management• Immediate Medical Attention
– Ensure airway is patent– Give oxygen to offset cerebral hypoxia– Give intravenous anticonvulsants (Like Diazepam 10 mg) ONLY IF seizures are
continuous or repeated– Consider taking blood for anticonvulsants if patient is a known epileptic
• Anticonvulsant therapy– Begin with single drug of choice at low dosage, ↑ dosage over 4-6 weeks– If seizures are not controlled, ↑ dose to attain plasma level in upper part of
therapeutic range, until side effects are seen– If poorly controlled, change the drug into 2nd line of drug of choice, by
gradually decreasing the first drug in 3-4 weeks– Usually, 3 single drugs are tried before using combined therapy– NOTE: First seizure episode should not be followed by antiepileptic drug
therapy. Consider drugs after second or if repeated h/o seizures.
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Drugs of choice
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Types First line Second line Third line
Partial and/or secondary GTCS
Carbamazepine LamotrigineSodium valproateTopiramateTiagabineGabapentine
ClobazamPhenytoinPrimidonePhenobarbitalOxcarbazepineLevetiracetamVigabatrinAcetazolamide
Primary GTCS Sodium valproate LamotrigineTopiramateCarbamazepine
PhenytoinGabapentinePrimidonePhenobarbital
Absence Ethosuximide Sodium valproate LamotrigineClonazepamAcetazolamide
Myoclonic Sodium valproate Clonazepam PiracetamLamotriginePhenobarbital
Prognosis
• Generalized seizures are more readily controlled than partial seizures
• With 20 years of diagnosed epilepsy• 50% are free of seizures without continuing
medications since last 5 years• 20% are free of seizures with continuation of
medication• 30% Still continue seizing despite medical
therapy
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Status epilepticus
• LIFE THREATENING MEDICAL EMERGENCY• Series of seizures occur without the patient
regaining awareness between attacks• Recurrent tonic clonic seizures (Major status)
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Management of status epilepticus
• General measures• Immediate care (as discussed earlier)– IV access– Draw blood for glucose, electrolytes etc, save
some for other analysis– Inj Diazepam 10mg iv stat, repeat once after 15
mins– Transfer the patient to ICU for intensive Mn
• Pharmacological treatment
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Pharmacological treatment• If seizures continue after 30 mins
– IV infusion with one of the following drugs:• Phenytoin: iv 15mg/kg @ 50mg/min• Fosphenytoin: iv 15mg/kg @ 100mg/min• Phenobarbital: iv 10mg/kg at 100mg/min
• If seizures continue after 30-60 mins– Start Rx for refractory status with intubation and ventilation,
and general anesthesia with propofol or thiopental• Once status is controlled
– Commence longterm anticonvulsant therapy with one of:• Sodum Valproate 10mg/kg iv over 3-5 mins, then 800-2000mg/day• Phenytoin: give a loading dose of 15mg/kg, infuse at <50mg/min, then
300mg/day• Carbamazepine 400mg by NG tube, then 400-1200mg/day
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Antiepileptics in pregnancy
• Associated with congenital defects• Spina bifida, cleft lip, cardiac defects• Lamotrigine and gabapentine is supposed to
be comparatively safer • Pts are advised to use Folic acid 5mg daily 2
months prior to conception, which might reduce the risk of congenital deformity
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Partial
• Occurs within discreet portion of brain• Involuntary jerking of finger or hand
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Tonic clonic
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Complex partial
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Absence seizure
•
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Partial motor
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Partial sensory
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versive
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Partial visual
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Classification of Epilepsy
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