I. What every physician needs to know.

Partial seizures can also be known as focal seizures because by definition they start at a seizure focus, or at a certain part of the cerebral cortex that is irritated/injured. Partial seizures can generalize (generalized tonic-clonic seizure), and when they do, the actual generalized convulsion is indistinguishable from any other generalized convulsion (i.e. if it started generalized or if it spread to become generalized from any part of the brain).

Simple partial just means a focal seizure that stays small and does not alter consciousness. Complex partial means the seizure spread enough to alter consciousness. Note that complex partials do nothave to causetotal loss of consciousness.

Remember, seizures are synchronized electrical discharges from an irritated area of cerebral cortex, and epilepsy is the predilection to have recurrent and unprovoked (not caused by drug intoxication/withdrawal each time) seizures.

II. Diagnostic Confirmation: Are you sure your patient has Partial or Partial Complex Seizures?

The real diagnostic confirmation occurs if you capture the episode on EEG and confirm that it is a partial seizure. However, since that is difficult to do, focus on what occurs during the episode to define it as a partial seizure. Assuming that only one area of the brain is irritated and generating the seizure focus, the spells should be stereotyped (as in the same every time). What the patient does during the seizure is called the semiology, and semiology varies depending on where in the brain the seizure focus is.

See below for the specific patterns, but in general a partial seizure is characterized by a small positive neurologic symptom (twitching/movement, visual hallucination, abnormal behavior) that occurs for a brief period of time (30 seconds to 2 minutes). The more area of brain that is involved (more complex behavior and longer duration), the more alteration of consciousness there will be, culminating in a generalized tonic-clonic seizure if it spreads enough.

A. History Part I: Pattern Recognition:

Ask if the patient has a preceding aura, about seizure frequency, and any provoking factors. Partial seizures are categorized by where the seizure originates. The classic presentations are listed below.

  • Temporal lobe seizures (by far the most common)

  • – Oral (lip-smacking/chewing) automatisms

  • – Manual (fumbling/hand-picking/dystonic hand posturing) automatisms

  • – Head turning/eye version away from side of seizure focus

    Frontal lobe seizures

  • – Complex “hypermotor” activity (screaming/running/fighting) – overall very odd behaviors butkey isstereotyped/repetitive

    Parietal lobe seizures

  • – If involves more primary motor cortex, get focal motor seizure – focal twitching of hand/arm or foot/leg that may move as seizure expands (aka ‘Jacksonian march’)- If involves more primary sensory cortex, get focal paresthesias/tingling in the hand/arm or foot/leg

    Occipital lobe seizures

  • – Visual hallucinations, can be simple or complex

Key with all of the above is that the symptoms could have many different causes, but the stereotyped nature and intermittent recurrence should tip you off to consider seizure.

B. History Part 2: Prevalence:

Three percent of the general population will have a seizure at some point in their lifetime. Only a third of those will go on to develop epilepsy. For new onset seizures age >45, the causes are (in order of frequency) ischemia, tumor, trauma, infection. Seventy percent of partial seizures come from the temporal lobe, 10-20% from the frontal lobe, the remainder equally split between parietal and occipital lobes.

C. History Part 3: Competing diagnoses that can mimic Partial or Partial Complex Seizures.

In general, if consciousness is altered by the partial seizure, then causes of syncope will be on the differential. In particular, tussive syncope (syncope after a fit of coughing) can have some twitchy activity that accompanies the syncope and can be mistaken for a seizure.

Remember that “ruling out” reasonable cardiac etiologies of syncope does not rule in neurologic ones. Partial seizures are a specific diagnosis and not a diagnosis of exclusion.

The most common diagnostic mistake is to confuse complex partial seizures (particularly temporal lobe seizures) for absence seizures. The key is that absence seizures are a form of generalized epilepsy and NEVER occur in adults unless they have had them since childhood. There is no such thing as adult-onset absence seizures.

Frontal lobe seizures, due to the odd behaviors, are confused for psychosis/psychiatric problems.

Parietal lobe seizures can be mistaken for stroke/TIA, but the key is that the parietal seizure gives positive symptoms (tingling, twitching) while stroke/TIA would give negative symptoms (numbness, weakness).

Occipital lobe seizures are often mistaken for psychosis/psychiatric disturbance, but remember that an older adult is unlikely to develop new onset schizophrenia but is much more likely to have a tumor or stroke irritating the occipital cortex to cause occipital lobe seizures.

D. Physical Examination Findings.

Unless the cause of the partial seizures is large (tumor/stroke) and causing other neurologic deficits, the exam is often completely normal.

E. What diagnostic tests should be performed?


1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

None if it is truly partial epilepsy, but if you suspect provoked seizures (or to rule out provoked seizures), then the typical labs to look for culprits would be an EtOH level, urine drug screen, and BMP.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

  • Routine EEG

  • – This is the most important test. If you obtain it during the event, of course that is the most helpful to capture the event electrographically, but even very soon after, you may see focal slowing in the leads over the part of the brain where the seizure had originated.

  • – Often an area of cortex irritated enough to be a seizure focus will have ‘inter-ictal discharges,’ or sharp waves in one/two leads indicating the underlying irritability.

  • – A single normal EEG does not rule out seizures, but repeatedly normal EEG’s makes seizures significantly less likely.

    Magnetic resonance imaging (MRI) brain w+wo contrast

  • – Do not bother with computed tomography (CT), as it does not give you sufficient resolution to see something in the parenchyma that may be a small seizure focus.

  • – If you do not get thin cuts through the hippocampi, then you may miss a small spot of hippocampal/mesial temporal sclerosis, which is the most common cause of temporal lobe epilepsy.

  • – MRI would also detect stroke/tumor/etc that may be the cause of the seizures.- If you cannot get MRI contrast, then a non-contrasted scan would still see mesial temporal sclerosis and stroke but not see tumor as well.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

As above, CT except to look for new blood in the head (trauma, suspect hemorrhagic stroke) is not helpful. If available, go straight to MRI to evaluate seizures.

Lactate is not helpful, as it may not be elevated at all in a partial seizure (usually requires a generalized tonic-clonic seizure to elevate the lactate) and even if it were elevated, then elevations lasts only 15 minutes or so.

III. Default Management.


A. Immediate management.

If the patient just had a partial seizure for the first time, then management is focused on finding out if it was a seizure and what might have been the incipient cause (workup above). If a patient is having recurrent partial seizures (aka epilepsy), then the key is selecting the right anti-epileptic drug (AED) therapy (see list below).

B. Physical Examination Tips to Guide Management.

If there is a post-ictal Todd’s paralysis even after a partial seizure, then this can give a clue to the seizure focus. You will still need imaging to clarify this though. Other exam findings are not useful unless they are pointing you to the localization of the seizure focus. If the cause at the seizure focus is reversible/treatable, then that treatment should be initiatied.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Certain AED’s may require lab testing for monitoring for side effects (see list below), but there are no lab tests for the seizures themselves.

D. Long-term management.

If the patient has had recurrent partial seizures or a single partial seizure but there is reason to suspect that it would recur (you found a stroke or tumor in your workup, etc), then the long-term management is placing the patient on an AED for suppression of further seizures. A single partial seizure should not receive IV benzos (Ativan/Valium) unless it progresses to a generalized tonic-clonic seizure. Provoked seizures do NOT require treatment – simply remove the provoking agent. Withdrawal, intoxication, and metabolic disturbance all most commonly cause provoked generalized seizures but can rarely cause provoked partial seizures.

E. Common Pitfalls and Side-Effects of Management.

  • Evaluate for the cause of the partial seizures as above

  • – EEG

  • – MRI

  • Treat the partial seizures using AED’s if single seizure with structural cause (stroke/tumor) or recurrent

  • – Best AED’s for partial seizures (in order of efficacy): Carbamazepine, oxcarbazepine, phenytoin, lamotrigine, topiramate, levetiracetam, zonisamide, valproate

    AED’s – only the ones marked by * are available IV

    Carbamazepine (other formulations: Tegretol XR, Carbatrol)

  • – For generic carbamazepine start 200mg TID titrate to 400mg TID, Tegretol XR and Carbatrol can be dosed BID; SE’s: commonly get hyponatremia, may have N/V, dizziness, diplopia, rarely agranulocytosis or aplastic anemia; Check q6 month CBC, BMP, carbamazepine level; P450 inducer and can induce its own metabolism with rapid titration;therapeutic level 4-12

    Oxcarbazepine( Trileptal )

  • – Start 300mg qHS, titrate to 450-600mg BID, very similar to Tegretol except generally felt to be better tolerated (fewer side effects), but still must watch for hyponatremia

    *Phenytoin Dose

  • – Start 300mg daily; SE’s: gingival hyperplasia, hirsutism, osteoporosis long term and ataxia/nystagmus when supratherapeutic; Check LFT’s including albumin with drug levels (therapeutic 10-20), since if albumin low, corrected level much higher

  • – Re-loading formula (if level <10): IV Loading dose (in mg/kg) = [Goal level – curr. level] x 0.7

  • – Corrected Phenytoin Level: [Measured level] / (0.2 x albumin + 0.1)


  • – Highest incidence of Stevens-Johnson (related to speed of titration), titrate dose slowly (start 25mg daily, titrate weekly up to 100mg BID, though titration adjusted based on whether or not on other AED’s), one of the safest in pregnancy (so far), is the least cognitively interfering

    Topiramate (Topamax)

  • – Start 25mg BID, titrate weekly to 200mg BID, watch for kidney stones, wt. loss, cognitive slowing, mild carbonic anhydrase inhibitor; cognitive effects improved by slowing speed of titration

    *Levetiracetam (Keppra)

  • – Start 500mg BID, titrate to max of 2000-2500mg/day, renally cleared, no hepatic metabolism so no drug interactions, few SE’s (most common is behavioral change/irritability)

    Zonisamide (Zonegran)

  • – Start 100 qHS, can titrate to 600mg max, cannot take if allergic to sulfa, also a carbonic anhydrase inhibitor, half life 60 hrs; has similar side effects to Topamax but milder; available as a generic


  • – Preferred is starting ER 250mg BID and titrating to 500mg BID; Common side effects include significant wt. gain with obesity (occurs in 30-50% of pts taking it), hair loss, bruising, and tremor but also may rarely have hepatotoxicity and thrombocytopenia. Also the most teratogenic with ~7% incidence of neural tube defects in some studies. Check LFT’s, CBC, level q 6 mos.Therapeutic level 50-100

IV. Management with Co-Morbidities.


A. Renal Insufficiency.

Depending on the AED chosen (primarily levetiracetam), may need to decrease the dose.

B. Liver Insufficiency.

Depending on the AED chosen (phenytoin, carbamazepine, valproate), may need to decrease the dose.

C. Systolic and Diastolic Heart Failure.

No change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease.

No change in standard management.

E. Diabetes or other Endocrine issues.

Avoid valproate, which has known endocrine side effects and causes weight gain.

F. Malignancy.

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD).

No change in standard management.

I. Gastrointestinal or Nutrition Issues.

Hypermotility syndromes will decrease blood levels of most AED’s.

J. Hematologic or Coagulation Issues.

No change in standard management.

K. Dementia or Psychiatric Illness/Treatment.

Some AED’s have mood-stabilizing properties, which can be an added benefit.

V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

If only partial seizures, can sign out not to keep giving IV benzos to the patient.

B. Anticipated Length of Stay.

Patients do not typically need inpatient admission just for eval/starting treatment, but tests can be completed in one day. Choice of AED will determine length of titration, but patient can be discharged after 1 day on the AED to document tolerability.

C. When is the Patient Ready for Discharge.

When workup is complete. Ideally seizure free for 24 hours is discharge criteria, but if seizure frequency is high (multiple times a day or more), then it may not be feasible to totally stop the seizures during the admission.

D. Arranging for Clinic Follow-up.


1. When should clinic follow up be arranged and with whom.

If workup not completed as an inpatient, then patient needs follow-up in 1-2 weeks in neurology, preferrably with an epilepsy specialist. If the patient did have a workup and was started on an AED, then the patient should follow up within 1 month in neurology.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

EEG for sure, MRI if available.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Possibly repeat EEG if the first one in the hospital was unrevealing.

E. Placement Considerations.


F. Prognosis and Patient Counseling.

If a structural lesion (stroke, tumor, mesial temporal sclerosis) is found as the cause of the partial seizures, then they may prove refractory without attempts at surgical resection of the seizure focus. If the patient with partial seizures and the above structural lesion fails adequately dosed trials of three medications, then the likelihood ofever achieving seizure control with medications is less than 10%.

For counseling, if the patient has complex partial seizures (altered consciousness), then he/she should be counseled according to the local state law (usually state no driving after episode of unexplained altered consciousness until spell-free for X number of months).

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Most common reason for readmission is increasing seizure frequency. Patient needs close followup after discharge to assure that seizures are controlled on your medication regimen.

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