1. LAPSS causes :
LOS ANGELES PREHOSPITAL STROKE SCREEN
cerebrovascular accident =CVA
ALL 6 MUST BE POSITIVE thrombosis, embolism, hemmorhage
>45 YEARS OLD
NO PRIOR SEIZURE HISTORY transient ischemic attack = TIA
NEW ONSET OF NEUROLOGIC SYMPTOMS IN 24 HOURS
WAS AMBULATORY AT BASELINE PRIOR TO EVENT migraine syndrome
BLOOD GLUCOSE RANGE = 60 - 400 todd's paralysis
UNILATERAL ASYMMETRY
FACIAL DROOP
GRIP WEAKNESS / ABSENCE vasculitis
ARM WEAKNESS
nonketotic hyperosmolar coma
SENSITIVITY = 93#
SPECIFICITY = 97 % head trauma
brain contusion
subdural hematoma
epidural hematoma
hemiplegia = paralysis
hemiparesis = weakness infection
brain abscess
encephalitis
symptoms subdural empyema
sudden unilateral extrimity weakness, loss of function meningitis
= spinal cord or higher involvement
demyelinating disease
signs multiple sclerosis
cortical lesion = depends on dominant hemisphere acute necrotizing myelitis
subcortical, brainstem, spinal cord = the same
hereditary disease
dominant leykodystrophies
aphasia
cortical sensory loss congenital or perinatal injury
nondominant
inattention = neglect dysphagia
denial 55% of CVA, 40 - 70% silent aspiration
constructional apraxia
1 or less = mild or no dysphagia
spatial siorientation
2 or more = moderate to severe
dysphonia, dysarthria, abnormal gag reflex,
cough 1 min after water ingestion,
voice change after swallow 5, 10, 20 cc
neurologic exam
face [ cranial nerves, palpebral fissures equal, fascial symmetry, tongue midline no fasciculations,
jaw symmetric ]
oropharynx [ gag reflex, swallow reflex, regurgitation : nasal or liquid ]
larynx and language [ voice quality, speech exam, dysarhria [ explosive or nasal ]]
sensory exam [ two point dicrimination, sharp and dull discrimination, propioception [ down or up?]]
motor exam [ strenght, tone[flaccid, rigid, cogwheel], atrophy, fasciculations, tenderness, tremor ]
cerebellum [ dysmetria = finger nose, romberg ]
gait patterns
vestibular exam
reflexes [ deep tendon -- primitive [babinski, grasp, suck, glabellar, hoffman]]

2. Todd's paresis
From Wikipedia, the free encyclopedia
Todd's paresis or Todd's paralysis (or postictal paresis/paralysis, "after Todd's paresis
seizure") is focal weakness in a part of the body after a seizure. This
weakness typically affects appendages and is localized to either the left or ICD-10 G83.8
right side of the body. It usually subsides completely within 48 hours. ICD-9 344.89
Todd's paresis may also affect speech, eye position (gaze) or vision.
MeSH D010243
The condition is named after Robert Bentley Todd (1809-1860), an Irish-
born London physiologist who first described the phenomenon in 1849.[1][2]
It may occur in up to 13% of seizure cases.[3] It is most common after generalised tonic-clonic seizures ("grand mal"), and may
last for hours or occasionally days after the initial seizure. The generally postulated cause is the exhaustion of the primary
motor cortex, although no conclusive evidence is available to support this.
Contents
 1 Presentation
 2 Causes
 3 Treatment
 4 Prognosis
 5 Importance
 6 References
Presentation
The classic presentation of Todd's paresis is a transient weakness of a hand, arm, or leg after
partial seizure activity within that limb. The weakness may range in severity from mild to
complete paralysis.
When seizures affect areas other than the motor cortex, other transient neurological deficits
can take place. These include sensory changes if the sensory cortex is involved by the seizure,
visual field defects if the occipital lobe is involved, and aphasia if speech, comprehension or
conducting fibres are involved.
Todd's paresis, as defined as any motor deficit after seizure, occurs in 13% of all seizures.[3]
This was evaluated in a study of 513 patients with epilepsy with video-
electroencephalography. The same study also showed that the mean duration of postictal
paresis was 173 seconds, with ranges of 11 seconds to 22 minutes.[3] There have been case
Robert Bentley Todd
reports of longer durations of paresis, ranging to as long as days.[4]
Other post-ictal neurological findings that do not involve activity of the area affected by the seizure have been described. They
are thought to be caused by a different mechanism than Todd's paresis, and including paralysis of the contralateral limb,[5] and
rare genetic causes of hemiplegia and seizures.[6]
Todd's paresis is more common after any clonic seizure activity, and particularly if generalized tonic-clonic seizures occur.[3]
Causes
The cause of Todd's paresis is unknown but there are two hypotheses to its cause. The first is the depletion theory, where the
motor cortex is exhausted leading to prolonged neuronal hyperpolarization. The second is that there is transient inactivation of
motor fibres caused by activation of NMDA receptors. Neither has been extensively evaluated.

3. Treatment
Treatment of Todd's paralysis is symptomatic and supportive because the paralysis disappears quickly.
Prognosis
An occurrence of Todd's paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects
of the seizure, not the occurrence of the paralysis.
Importance
The most significant issue regarding the Todd's paresis is its differentiation from a stroke. The issue is further complicated by
the fact that some strokes trigger a focal seizure during the acute phase. A Todd's paresis in this context may overestimate the
extent of neurological deficit due to the vascular process itself resulting in erroneous decisions with regards to acute stroke
therapy such as thrombolysis. For this reason a seizure during an acute stroke is generally accepted to be a relative
contraindication to thrombolytic therapy, especially in the absence of documented cerebrovascular occlusion using vascular
imaging techniques.[7]
An infant with Todd's paresis does not necessarily preclude the diagnosis of a febrile convulsion. This view is as a result of a
recent study that showed the incidence of Todd's paresis to be in 0.4% of infants that have been diagnosed with a febrile
convulsion.[8]
References
1. ^ Todd RB (1849). "On the pathology and treatment of convulsive diseases". London Med Gaz 8: 668.
2. ^ Pearce JM (March 1994). "Robert Bentley Todd (1809-60) and Todd's paralysis". J. Neurol. Neurosurg. Psychiatr. 57 (3): 315.
doi:10.1136/jnnp.57.3.315. PMID 8158178.
3. ^ a b c d Gallmetzer P, Leutmezer F, Serles W, Assem-Hilger E, Spatt J, Baumgartner C (June 2004). "Postictal paresis in focal
epilepsies--incidence, duration, and causes: a video-EEG monitoring study". Neurology 62 (12): 2160–4. PMID 15210875.
4. ^ Kimura M, Sejima H, Ozasa H, Yamaguchi S (1998). "Technetium-99m-HMPAO SPECT in patients with hemiconvulsions
followed by Todd's paralysis.". Pediatr Radiol 28 (2): 92–4. doi:10.1007/s002470050300. PMID 9472051.
5. ^ Oestreich L, Berg M, Bachmann D, Burchfiel J, Erba G (1995). "Ictal contralateral paresis in complex partial seizures.". Epilepsia
36 (7): 671–5. doi:10.1111/j.1528-1157.1995.tb01044.x. PMID 7555983.
6. ^ Mikati M, Maguire H, Barlow C, Ozelius L, Breakefield X, Klauck S, Korf B, O'Tuama S, Dangond F (1992). "A syndrome of
autosomal dominant alternating hemiplegia: clinical presentation mimicking intractable epilepsy; chromosomal studies; and
physiologic investigations.". Neurology 42 (12): 2251–7. PMID 1361034.
7. ^ Sylaja PN, Dzialowski I, Krol A, Roy J, Federico P, Demchuk AM (2006). "Role of CT angiography in thrombolysis decision-
making for patients with presumed seizure at stroke onset". Stroke 37 (3): 915–7. doi:10.1161/01.STR.0000202678.86234.84. PMID
16456124. http://stroke.ahajournals.org/cgi/content/full/37/3/915.
8. ^ Nelson K,Ellenberg J; Prognosis in Children With Febrile Seizures Paediatrics; 61, 5: 720-727
Retrieved from "http://en.wikipedia.org/wiki/Todd%27s_paresis"
Categories: Neurology
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4. NINDS Todd's Paralysis Information Page
Synonym(s): Epileptic Hemiplegia
Table of Contents (click to jump to sections)
What is Todd's Paralysis?
Is there any treatment?
What is the prognosis?
What research is being done?
Clinical Trials
Organizations
What is Todd's Paralysis?
Todd's paralysis is a neurological condition experienced by individuals with epilepsy, in which a seizure is followed by a brief
period of temporary paralysis. The paralysis may be partial or complete but usually occurs on just one side of the body. The
paralysis can last from half an hour to 36 hours, with an average of 15 hours, at which point it resolves completely. Todd's
paralysis may also affect speech and vision. Scientists don't know what causes Todd's paralysis. Current theories propose
biological processes in the brain that involve a slow down in either the energy output of neurons or in the motor centers of the
brain. It is important to distinguish Todd's paralysis from a stroke, which it can resemble, because a stroke requires completely
different treatment.
Is there any treatment?
There is no treatment for Todd's paralysis. Individuals must rest as comfortably as possible until the paralysis disappears.
What is the prognosis?
Todd's paralysis is an indication that an individual has had an epileptic seizure. The outcome depends on the effects of the
seizure and the subsequent treatment of the epilepsy.
What research is being done?
The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to Todd's paralysis in its clinics
and laboratories at The National Institutes of Health (NIH), and supports additional research through grants to major medical
institutions across the country. Much of this research focuses on finding successful methods to prevent Todd's paralysis in
individuals with epilepsy.
NIH Patient Recruitment for Todd's Paralysis Clinical Trials
At NIH Clinical Center
Throughout the U.S. and Worldwide
Organizations
Epilepsy Foundation
8301 Professional Place
Landover, MD 20785-7223
postmaster@efa.org
http://www.epilepsyfoundation.org
Tel: 301-459-3700 800-EFA-1000 (332-1000)
Fax: 301-577-2684
Prepared by:
Office of Communications and Public Liaison
National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892
NINDS health-related material is provided for information purposes only and does not necessarily represent endorsement by or an

5. official position of the National Institute of Neurological Disorders and Stroke or any other Federal agency. Advice on the
treatment or care of an individual patient should be obtained through consultation with a physician who has examined that patient
or is familiar with that patient's medical history.
All NINDS-prepared information is in the public domain and may be freely copied. Credit to the NINDS or the NIH is appreciated.
Last updated September 16, 2008
National Institute of Neurological Disorders and Stroke
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