Neurosurgery notes/Functional/Seizure

Seizure

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Parent item
Functional
Sub-item
Nonepileptic seizures
Work-up of seizures
Semiology
Seizure classification
Outcome scale
Status epilepticus (SE)
Anti epileptic medication
Sudden Unexpected Death in Epilepsy (SUDEP)

Definition

Seizure

  • An abnormal paroxysmal cerebral neuronal discharge that results in alteration of sensation, motor function, behaviour, or consciousness.

Unprovoked seizures

  • Seizures occurring in the absence of precipitating factors and may be caused by a static injury or a progressing injury
  • Can be single or recurrent
  • One unprovoked seizure has a >60% of developing another seizure in the next 10 years

Symptomatic seizures

  • Progressive injuries:
    • Unprovoked seizures owing to progressive central nervous system disorders
    • Eg: tumour or degenerative disorder
  • Static injuries:
    • Seizure that occurs longer than 1 week following a disorder that is known to increase the risk of developing epilepsy
    • Eg: Traumatic brain injury, cerebrovascular disease, drug withdrawal, infarction, and metabolic insults
  • Remote symptomatic seizure:
    • A seizure that occurs longer than 1 week following a disorder that is known to increase the risk of developing epilepsy.

Epilepsy

  • 2 or more recurrent seizures unprovoked by systemic or actuate neurologic insults
  • A disorder of recurrent seizures
  • Febrile seizures are not epilepsy).
  • Types:
    • Focal
      • Depends on origin of seizure
      • +/- impaired consciousness
      • +/- becoming generalised
    • Generalised
      • Tonic
      • Clonic
      • Tonic-Clonic
      • Atonic
      • Myoclonic
      • Absence

Drug Resistant Epilepsy: (ILAE-Kwan 2010)

  • Not responding to 2 agents for more than 6 months

Numbers

Hauser 2008

  • Worldwide:
    • Incidence of acute symptomatic seizures is 29–39/100,000 per year
    • SMR (standardized mortality ratio): ratio of observed deaths in the study group to expected deaths in the general population
      • Single unprovoked seizure: 2.3
      • Newly diagnosed unprovoked seizure 2.5 to 4.1 [(2.5-1)*100] 150% more death than general population}
  • UK: (n=100,230)
    • Unprovoked (single and recurrent) seizure incidence: 57.0/100,000
    • Single unprovoked seizures: 11.0/100,000

Paeds

  • ONS
    • Prevalence of epilepsy 1%
    • Incidence of paeds epilepsy: 51/100000/yr
  • Berg et al 2009
    • Medically refractory: 12.7/100 ooo/yr
    • Surgically remediable: 2.7/100 ooo/yr (350 UK cases/ yr )
  • Of 56 patients actually thought to have had a first-time seizure (Landfish 1992)
    • 71% were febrile seizures
    • 21% were idiopathic
    • 7% were symptomatic

Adults

  • 244 patients with a new-onset unprovoked seizure, only 27% had further seizures during follow-up
  • Rule of 5
    • Life time risk: 5%
    • Incidence: 0.5%
    • Prevalence: 0.5%
    • Mortality: 0.5%
  • Medically refractory seizures 20-40% of all patients with epilepsy

General

Todd’s paralysis

  • A post-ictal phenomena in which there is partial or total paralysis usually in areas involved in a partial seizure.
  • More common in patients with structural lesions as the source of the seizure.
  • The paralysis usually resolves slowly over a period of an hour or so.
  • Due to depletion of neurons in the wake of the extensive electrical discharges of a seizure.
  • Other similar phenomena include
    • Post-ictal aphasia
    • Post ictal hemianopsia.

Predictors for low probability of epilepsy remission

  • Symptomatic localized epilepsy secondary to remote CNS injury,
  • Abnormalities on neurological examination or developmental delay,
  • Persistent epileptiform abnormalities on EEG,
  • Older age at onset
  • Inadequate control of seizures for longer than 4 years,
  • Presence of multiple seizure types and frequent generalized tonic-clonic seizures.
  • Seizure duration of over 10 years also decreases likelihood of achieving seizure control in those who undergo epilepsy surgery.

Nomenclature

Primary generalized seizure

  • Bilaterally symmetrical and synchronous, involving both cerebral hemispheres at the onset, no local onset, consciousness lost from the start.
  • Generalized tonic clonic: Grand-mal seizure
    • Generalized seizure that evolve from tonic → tonic clonic
    • Does not include partial seizures that generalize secondarily
  • Clonic seizures: fairly symmetric, bilateral synchronous semirhythmic jerking of the UE & LE, usually with elbow flexion and knee extension
  • Tonic seizures:
    • Sudden sustained increased tone with a characteristic guttural cry or grunt as air is forced through adducted vocal cords
  • Absences (petit-mal seizures): Impaired consciousness with mild or no motor involvement
    • Typical
    • Atypical
      • Last longer
      • More heterogenous with more variable EEG pattern
  • Myoclonic
    • Shock like body jerks with generalized EEG discharges
  • Atonic (drop attacks)
    • Sudden brief loss of tone that causes falls

Partial seizure

  • Simple partial
    • No impairment of consciousness
    • w/
      • Motor signs (jacksonian)
      • Sensory symptoms
        • Special sense
        • Somatosensory
      • Autonomic signs or symptoms
      • Psychic symptoms
  • Complex partial
    • Any alteration of consciousness,
      • LOC or
      • Automatisms (including lip smacking, chewing, or picking with the fingers)
    • With autonomic aura (usually an epigastric rising sensation)
    • Types
      • Simple partial onset followed by impairment of consciousness (may have premonitory aura)
        • Without automatisms
        • With automatisms
      • With impairment of consciousness at onset
        • Without automatisms (impairment of consciousness only)
        • With automatisms
      • Partial seizure with secondary generalization
        • Simple partial evolving to generalized
        • Complex partial evolving to generalized
        • Simple partial evolving to complex partial evolving to generalized

Factors that inc. seizure risk

Modifiable

  • Sleep deprivation
  • Hyperventilation
    • Hyperventilation → reduce paCO2 → respiratory alkalosis → increases the pH → inc membrane excitability → induce seizures.
  • Photic stimulation (in some)
  • Infection
    • Systemic (febrile seizures),
    • CNS (meningitis…)
  • Metabolic disturbances:
    • Electrolyte imbalance (especially profound hypoglycemia),
    • pH disturbance (especially alkalosis),
    • Drugs
      • Medications frequently used in neurosurgery that can lower seizure threshold
        • Antidepressants: Baclofen, phenytoin at supratherapeutic levels
        • Analgesics: Meperidine, fentanyl, and tramadol
        • Anesthetics: Methohexital and enflurane
        • Benzodiazepines
        • Barbiturates and withdrawal of antiepileptic drugs
        • Antibiotics: Cefazolin, imipenem, and metronidazole
        • Radiographic contrast materials
  • Head trauma: closed head injury, penetrating trauma
  • Cerebral ischemia: stroke (see below)
    • Excessive oxidative stress
      • Fenton and Haber-Weiss reaction in triggering epilepsy
        • Generates •OH (hydroxyl radicals) from H₂O₂ (hydrogen peroxide) and superoxide (•O₂⁻).
            • The first step of the catalytic cycle involves reduction of ferric ion to ferrous:
              • Fe³⁺ + •O₂⁻ → Fe²⁺ + O₂
            • The second step is the Fenton reaction:
              • Fe²⁺ + H₂O₂ → Fe³⁺ + OH⁻ +•OH
            • Net reaction:
              • •O₂⁻ + H₂O₂ → •OH + HO⁻ + O₂
            notion image
  • 2nd seizure

Nonmodifiable

  • “Kindling”: a concept that repeated seizures may facilitate the development of later seizures
  • A family seizure history,
  • Spike-and-waves on EEG

Evaluation

Adults

  • Idiopathic seizure occurs generally before or during adolescence → new onset without obvious cause (Etoh withdrawal) MUST be investigated
  • Investigate:
    • Bloods
    • CT +/-C
    • MRI +/- C
    • If still no cause found repeat CT or MRI in 6 months, 1 year and 2 years → r/o tumour

Paeds for 1st time seizures

  • History & Physical exam more important than blds and radiological
  • Presurgical evaluation
      • notion image

Causes

Reference

Subarachnoid haemorrhage

  • There is insufficient evidence to provide a definitive duration of AED treatment (or even if AEDs should be used prophylactically) in patients following subarachnoid haemorrhage.
  • If AEDs are started, early discontinuation after securing any vascular abnormality is likely safe and beneficial. AEDs should not be routinely continued after recovery from subarachnoid haemorrhage

Brain tumour

  • Perioperative AED prophylaxis for brain tumour surgery provides a statistically significant reduction in early (within the first postoperative week) postoperative seizure risk
  • Evidence on the timing and rate of AED withdrawal in the context of adult brain tumours is also limited but it appears that after 1-2 years of seizure freedom drug withdrawal may be appropriate.
  • Any tumor can be a possible cause of seizures. In the setting of chronic epilepsy, tumors represent 25% to 35% of the cases
  • In young adults and children, the most common tumors associated with epilepsy are dysembryoplastic neuroepithelial tumors (DNETs) and gangliogliomas

Prophylaxis in Brain Tumours and Mets

  • More than 1/3 of of primary brain tumors present with epileptic seizures
  • Patients who have not experienced a seizure remain at risk, however, and at least 20% to 45% ultimately develop seizures.
  • American Academy of Neurology
    • In patients with newly diagnosed brain tumors anticonvulsant medications are not effective in preventing first seizures and should therefore be avoided
    • In patients with brain tumors who have not had a seizure, tapering and discontinuing anticonvulsants after the first post-operative week is appropriate

Vascular malformation

  • Axial T2 and gradient echo sequence showing classical ‘popcorn’ appearance Hemosiderin stain (arrows) highlighted by gradient echo sequence
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Other lesions

  • Encephalocele
      • notion image
      notion image
      • Encephaloceles can be associated with other features suggesting altered CSF dynamics such as:
          • (A) Enlargement of CSF spaces
          (B) Enlarged pituitary fossa
          (C) Prominent optic sheaths
      Fig. A
      Fig. A
      Fig. B
      Fig. B
      Fig. C
      Fig. C

Clinical assessement

  • History from patient
  • History from eve witness - VITAL
  • Need detailed history of:

      • Background/provoking factors

      • Previous or family history
      • Early life risk factors
        • Birth injury, febrile convulsions, meningitis, encephalitis
      • Brain injury: stroke, neurosurgery
      • Myoclonic jerks in / since teens
      • Provoking factors
        • Change in alcohol, drugs, sleeping tablets
        • Sleep deprivation

      Preceding symptoms

      • Generalised
        • Usually no warning
      • Focal – ‘Aura’
        • Strange taste, smell
        • Déjà-vu, jamais-vu
        • Fear
        • Ascending unusual feeling
        • Sensory changes

      Description of attack – witness! seizures

      • Focal seizures
        • Automatisms → temporal lobe symptoms
          • Oro-facial (lip smacking)
          • Manual (picking, stroking)
        • Head and eye deviation
        • Limb stiffening/jerking
        • Reduced interaction or responsiveness
        • Duration
          • Frontal lobe 10-20 seconds
          • Temporal lobe 2-4 minutes
      • Generalised seizures
        • Body stiff, rigid, crashing to ground
        • Often letting out loud scream
        • From rigid to rhythmical limb jerking (not tremor)
        • Colour purple/blue (as if dead)
        • Eyes often open (rolled back)
        • Lasts 1-2 minutes, then jerking slows down
        • Often heavy breathing, snoring

      After event

      • Witness
        • Non-responsive for some minutes
        • Often post-ictal confusion
        • Dysphasia, Todd’s palsy (if focal onset)
      • Patient
        • May not recall events or extremely delayed
        • Headache
        • Achey all over (myalgia)
        • Goes to sleep it off

Outcomes of drug resistant epilepsy

Classification of Malformations of Cortical Development (MCDs)

  • 3 groups:

      • Group 1

      • Malformations resulting from abnormal proliferation of neuronal and glial cells.
      • Focal cortical dysplasia without and with balloon cells (Taylor dysplasia types IIa and IIb, respectively)
      Review the images in the context of seizure semiology and EEG findings
      Review the images in the context of seizure semiology and EEG findings

      Group 2

      • Malformations resulting from abnormal neuronal migration.
      • Types of group 2 malformations
        • Heterotopias
            • Presence of grey matter in abnormal sites
            • A&B: Coronal T1 and axial T2 weighted image showing extensive bilateral subependymal nodular gray matter heterotopia
            • C: Coronal T1 weighted image showing band heterotopia in the right cerebral hemisphere
            notion image
        • Lissencephaly
            • Smooth brain appearance
            • Axial T2 weighted image: brain appears agyric with shallow sulci and thickened cortex
            notion image

      Group 3

      • Malformations resulting from abnormal cortical organization.
      • Types of group 3 malformations
        • Polymicrogyrias
        • Schizencephaly
            • Coronal T1 weighted image showing schizencephaly reaching the right ventricle
            notion image
  • To be sorted
      • notion image