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Differential Diagnosis 1 – Weeks 3 & 4. Seizures.

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seizures
Seizures

Although approximately 6% of adults will experience at least one afebrile seizure in their lifetime, only 0.5% will have recurring seizures (epilepsy) (So and Hauser ref). This must be considered prior to initiating medical management decisions.

So NK. Recurrence, remission, and relapse of seizures. Cleve Clin J Med 1993;60:439-443.

Hauser WAS, Rich SS, Annegers JF, Anderson VE. Seizure recurrence after a 1st unprovoked seizure: an extended follow-up. Neurology 1990;40:1163-1167.

Twenty-four percent of epileptic patients are elderly with 38% of new cases occurring in the elderly (with stroke accounting for one-third of cases). (Stephen ref)

Stephen LJ. Epilepsy in elderly people. Lancet 2000;355:4-8.

seizures or convulsions
Seizures or Convulsions
  • Was there a hypoxic event?
    • Distinguish syncope from epileptic event
  • Occur only with fever?
  • Use or sudden withdrawal from prescribed or ilicit drug?
  • Family and personal history of attacks?
  • Search for localizing signs and individual triggers
age relationship to seizures
Age-Relationship to Seizures

Infancy- childhood: developmental, infection, trauma, cerebrovascular disease (CVD)

Adult – brain tumor, trauma, developmental disorder, infection, CVD

Late adulthood-elderly: CVD, brain tumor, degenerative disease, trauma

theories
Theories
  • Neurogenesis – based on animal models it appears that seizures can trigger increased mitotic activity in the dentate gyrus (specific to temporal lobe epilepsy) increasing differentiation and creation of new dentate granule cells
  • Mousy-fiber sprouting – found with temporal lobe epilepsy. These extend to pyramidal neurons as part of the hippocampal output pathway.
slide9

Cortical malformations – may be involved with partial or generalized epilepsy.

  • Theory is based on a disruption of development in the cerebral cortex classified as disorders of neuronal proliferation, neuronal migration, or disruption or re-organization of the cortex.
  • These may be involved more with refractory epilepsy and specifically in cases once believed to be cryptogenic.
  • Neurons within dysplastic areas may lack potassium channels or GABA-mediated inhibitory mechanisms.
slide10

Glial cell – glial cells, although primarily supportive, also serve functions of buffering that help maintain uptake of potassium and glutamate (among other metabolic balances). The result may be increased levels of extracellular potassium decreasing the threshold for neuronal firing (hyeprexcitability).

  • Chang BS, Lowenstein DH. Epilepsy. N Engl J Med 2003;349:1257-1266.
slide11

Table C30-1. Loci of origin of simple focal seizures

  • Motor - Movement of any part of the motor homunculus, sometimes with aphasia
  • Somatosensory - Contralateral numbness or tingling of face, fingers, or toes
  • Primary visual cortex - Flashes of light or patches of darkness in contralateral visual field
  • Visual association cortex -Twinkling light images in contralateral visual field
  • Basal occipitotemporal junction - Formed visual images of people or places, sometimes accompanied by sounds
  • Superior temporal gyrus (unusual) - Tinnitus, sometimes garbled word sounds
slide12

The Normal Thalamocortical Circuit and EEG Patterns during Wakefulness, Non-Rapid-Eye-Movement (Non-REM) Sleep, and Absence Seizures

Chang B and Lowenstein D. N Engl J Med 2003;349:1257-1266

medical treatment possible side effects
Medical Treatment & Possible Side-Effects

Valproic acid (Depacon) – tremor and weight gain

Phenytoin (Dilantin)– in young patients gingival hyperplasia and hirsutism

Carbamazapine (Carbatrol, Tegretol, Tegretol-XR) and oxcarbazepine (Trileptal) - hyponatremia in patients who drink large amounts of fluids or on diuretics

other tx options
Other Tx Options

Various surgical options – usually for those with a well-defined structural lesion

Vagal nerve simulation

Deep brain stimulation

Ketogenic diet

surgical options
Surgical Options

For refractive epilepsy there are several options dependent on the type, age, location and type of lesion. Following is a list of current surgical options with related types that may be treated (Nguyen ref):

Resective surgery – the epiloptogenic area must be delineated using several approaches to a convergent localization that allows accuracy in resection. Temporal lobe epilepsy is one example of epilepsy that may be responsive to resection.

Multiple Subpial transactions – based on the knowledge that functional cortical organization is primarly vertical. Intracortical fibers that are generally responsible for seizures are horizontally oriented. Small parallel cortical slices are made perpendicular to the long axis of the gyrus in an effort to spare function. This procedure is used alone or in combination with resective surgery for seizures arising in or around motor, sensory, or language cortical areas.

Gamma-Knife surgery – This is a stereotactic delivery of radiation to a very specific point in the brain which has been identified using MRI. There is a delay effect in results that may occur as much as one to three years post-procedure. Currently, three types of epilepsy are being evaluated for success using this treatment including hypothalamic hamartomas, vascular malformations, and mesial temporal lobe sclerosis. In selected cases, success rates for cessation of seizures is around 75%.

options for epilepsy
Options for Epilepsy
  • Vagal nerve stimulation – this is an adjunctive therapy with an effect of desynchronizing the EEG the left vagal nerve stimulation through a subcutaneous lead. The device may decrease frequency of seizures by about 25% but is not used as a cure-all.
  • Deep brain stimulation – stimulation of areas including the anterior thalamus, the cetromedian thalamic nucleus, the caudate nucleus, the posterior hypothalamus, and hippocampus have been experimented with. Multicenter studies are now underway to determine effectiveness.

Nguyen DK, Spencer SS. Recent advances in the treatment of epilepsy. Arch Neurol 2003;60:929-935.

types of memory
Types of Memory
  • Declarative (explicit) – facts, events
  • Nondeclarative (implicit) – skills and habits, priming, simple classic conditioning, nonassociate learning
  • Amnesia is an example of simple declarative loss; two types: antegrade and retrograde
  • Attention/Registration - < 1 sec.
  • Working – seconds to minutes
  • Consolidation – minutes to years
memory creation
Memory Creation

For long-term memory the postsynaptic cell needs to stimulate the manufacture of synapse-strengthening proteins (CREB proteins) that might then add more receptors or change the post-synaptic response in some way

Information that is declarative (people, places, events) must pass through the hippocampus before being recorded in the cerebral cortex.

primary causes and differences in adults
Primary Causes and Differences in Adults
  • Multi-Infarct Dementia - Sudden onset with associated neurological deficits that are often motor or sensory
  • Depression – memory loss is often profound; referred to as “pseudo-dementia” look for other indicators of depression
  • Age-Related Memory Loss – slow in onset, related only to learning new events (can’t teach an old dog new tricks)
  • Medication or Metabolic Related – relatively sudden onset timed with administration of medication or onset of other symptoms/signs; tested with laboratory
slide25

Alzheimer Disease

    • characterized by significant loss of memory and cognitive functions
    • subiculum and entorhinal cortex are among first sites where degenerative changes occur (hippocampus proper is also involved) relay of information through hippocampal formation is markedly affected
    • this damage is at least partially responsible for memory deficits seen in Alzheimer disease
    • Alzheimer’s is a progressive, neurological disease characterized by neurofibrillary tangles and plaques made of tau protein.
medical management
Medical Management

cholinesterase inhibitors (tacrine [Cognex] donepaxil [Aricept]) yet this tx does not alter the course of the disease

memantine, is an uncompetitive NMDA-receptor antagonist (anti-glutamatergic)

Aspirin may be preventive

Estrogen, Ginko-biloba, and memory games have been shown to have no effect

The only apparent effective therapy is aerobic exercise

references for aerobic exercise and the brain preliminary evidence
References for Aerobic Exercise and the Brain: Preliminary Evidence

Aerobic exercise training increases brain volume in aging humans.

Colcombe SJ, Erickson KI, Scalf PE, Kim JS, Prakash R, McAuley E, Elavsky S, Marquez DX, Hu L, Kramer AF.

J Gerontol A BiolSci Med Sci. 2006 Nov;61(11):1166-70.

Fitness effects on the cognitive function of older adults: a meta-analytic study.

Colcombe S, Kramer AF.

Psychol Sci. 2003 Mar;14(2):125-30.

slide28

Korsakoff Syndrome

    • condition caused by prolonged thiamine deficiency, typically seen in chronic alcoholics
    • causes a characteristic pattern of brain degeneration  typically mammillary bodies, dorsomedial nucleus of thalamus, and columns of fornix are involved  there is also loss of neurons in hippocampal formation
    • patients have short-term and long-term memory defects for events occurring since onset of disease  patients are prone to confabulations (string together fragments of memory from different events to form a “memory” of an event that never occurred)
    • in some patients it is accompanied by gaze palsies and ataxia secondary to cerebellar damage  Wernicke-Korsakoff syndrome
weakness
Weakness
  • Differentiate with questioning to determine a sense of fatigue or true muscular weakness
  • Neuro causes usually involve the distal extremities: determine if:
    • UMNL
    • LMNL
  • Muscular causes usually involve proximal muscle groups
  • Further differentiation may be needed with EMG/NCV
neurologic weakness
Neurologic Weakness
  • Neurologic weakness is painless weakness
  • Differentiate lower motor problems into either plexus, nerve root, or peripheral nerve problems
  • Plexus - diffuse symptoms/signs
  • Nerve root - dermatome, myotome, and sometimes deep tendon reflex effects
  • Peripheral nerve - specific group of muscles, patch of skin, possible DTR
  • Referred - no objective neurologic findings
slide32

The 3 M’s

Misunderstandings

Misconceptions

Myths

slide33

1

The mostcommon cause of cervical radiculopathyis

disc herniation

slide34

Approximately 80% of radicular presentations are due to

foraminal encroachment.

Only about 20% are due to a disc herniation

why not disc herniation as a cause in the cervical spine
Why not disc herniation as a cause in the cervical spine?

Protection from the PLL (posterior longitudinal ligament)

The location of the nerve roots/spinal nerve in the IVF

The loss of a nucleus pulposis by age 45

compression
Compression

Posterior IVF Compression

Fibrous tissue in IVF

Buckling of ligamentum flavum

Osteophytes from superior and inferior articular processes

slide37

2

Patients trace a dermatome when they have

nerve root involvement

slide38

Pain Patterns and Descriptions in Patients with Radicular Pain: Does the Pain Necessarily Follow a Specific Dermatome?Murphy DR, Hurwitz E, Gerrard JK, Clary RChiropractic & Osteopathy 2009; 17:9

except for c4
Except for C4 . . . .

Pain was non-dermatomal in 69.7% cases of cervicalradiculopathy

slide40

Except for S1 . . . .

Pain was non-dermatomal in 64.1% of cases of lumbarradiculopathy

slide41
Why?
  • A spinal segment does not equal all the nerves that goes to that spinal nerve
  • For example, sensory nerve fibers in the C5 spinal segment may not contribute to the C5 spinal nerve
  • Nerve fibers transmitting different sensory modalities to the same skin area may derive from different spinal nerves or different spinal segments
  • Overlap of innervaton from two spinal nerves may result in no loss of sensation when one is compressed or damaged
slide42

3

Patients claim weakness when they have

nerve root involvement

in subjects with electrodiagnostic evidence of radicuopathy
In subjects with electrodiagnostic evidence of radicuopathy . . . . .

64%-75% will have weakness on examination

Only 15%-34% will complainof weakness

in subjects with electrodiagnostic evidence of radicuopathy44
In subjects with electrodiagnostic evidence of radicuopathy . . . . .

Lauder TM. Physical Examination Signs, Clinical Symptoms, and Their Relationship to Electrodiagnostic Findings and the Presence of Radiculopathy. Phys Med Rehabil Clin N Am. 2002:451-467

31% will have no weakness on examination

33%-45% will have no sensory abnormalities

pronation strength for c6 c7
Pronation Strength for C6-C7

Although forearm flexion/wrist extension are used for C6 and elbow extension for C7, pronation is an option

For C6 – 72% had pronation weakness (wrist extension weak in 36%)

For C7 – 23% had pronation weakness with elbow extension weakness; pronation was only weakness in 10%

Rainville J, Noto DJ, Jouve C, Jenis L. Assessment of forearm pronation strength in C6 and C7 radiculopathies. Spine. Jan 1 2007;32(1):72-75.

slide46

4

The area of numbnessextends throughout the area of pain radiation

slide49

5

There is only one muscle that is found weak with each nerve root

slide52

6

Trauma is usually reported when cervical radiculopathy symptoms begin

slide53

Traumais reported in only 15% of cases of cervical radiculopathy

Radhakris K, Litchy WJ, O’Fallon Wm et al. Epidemiology of cervical radiculopathy: A population-based study from Rochestor, Minnessota, 1976 through 1990. Brain 1994;117:325-335.

slide54

7

Lumbar disc herniations compress the nerve root that is

exiting at that level

slide56

8

The straight leg raise is positive for nerve root involvement only from 30 to 70 degrees

the slr and what constitutes a positive
The SLR and What Constitutes a Positive

Jonsson B, Stromqvist B. Spine, 20(1), 27-30, 1995

Prior cadavericstudies indicated little dural tension until 30 degrees therefore positives below 30 degrees were not indicative of disc herniation as a cause of LBP

slide58

SLR positive in 42% of patients from 0-30 degrees

SLR positive in 26% of patients from 30-60 degrees

slide59

9

There is always radiation into the extremity with disc “rupture”

slide61

10

Most tests for cervical and lumbar nerve root involvement

are equal in ruling-in or ruling-out radiculopathy

localization of disc level based on signs symptoms
Localization of Disc Level Based on Signs & Symptoms

Kortelainen P, Puranen J, Koivisto e, et al. Spine 1985;10(1)88-92

  • L5-S1 disc rupture is 86% probable if three S1 signs are found:
    • pain projection to S1 area
    • pathologic Achilles reflex
    • sensory defect in S1 area

Pain projection into the S1 area is found with

all lumbar disc lesions including high levels

localization of disc level based on signs symptoms65
Localization of Disc Level Based on Signs & Symptoms
  • L4-L5 disc rupture 87% probable with three L5 signs:
    • extensor hallucis weakness
    • pain projection into L5 area
    • sensory defect of L5

With concomitant S1 findings accuracy of pain projection into L5 and EH weakness were still accurate

Extensor hallicus weakness and sensory defect in L5 area were 100% reliable for L4-L5 herniation

(When found)

slide69

Bottom Line

You can know when someone has a radiculopathy BUT

you can’t always know when they don’t