Seizure types Flashcards

1
Q

What are some of the typical features of seizures emanating from the mesial temporal lobes?

A

Features of mesial temporal lobe epilepsy: 1. “aura” - rising epigastric sensation - psychic or experiential phenomena (deja vu, fear) - gustatory or olfactory hallucination Auras can occur in isolation or can precede a focal seizure with impairment of consciousness 2. Focal seizures with impairment of consciousness or awareness - usually manifest with a behavioral arrest and staring and last between 30 and 120 seconds. 3. Automatisms - repetitive, stereotyped, purposeless movements. - ie hands (picking, fidgeting, fumbling) and mouth (chewing, lip smacking). 4. Lateralizing features can occur - Unilateral automatisms are usually ipsilateral to the seizure focus, - dystonic posturing almost invariably occurs on the contralateral side. - Head deviation at seizure onset is usually ipsilateral to the seizure; when it occurs later, it is contralateral 5. Postictal confusion usually resolves within minutes. Nose-wiping, performed by the hand ipsilateral to the focus of seizure onset, is a common postictal event in mesial TLE. 6. Heart rate changes commonly accompany temporal lobe seizures.

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2
Q

What are good and bad prognostic factors after temporal lobectomy? What is overall control like?

A

Good prognostic features after temporal lobectomy include presence of: - mesial temporal sclerosis on MRI of the brain (unilateraly), or presence of localized temporal lobe PET even if brain is NAD - a history of febrile seizures, - unilateral ictal and interictal EEG abnormalities. - presence of a focal brain lesion on MRI - shorter preoperative seizure duration ●Shorter preoperative seizure duration Comorbid psychiatric disease,has been associated with worse postsurgical seizure outcomes. Postoperatively, strongest predictor of long-term seizure control is freedom from seizures in the first year after surgery. The presence of interictal epileptiform discharges on an EEG performed within the first few years after surgery has been associated with an approximately threefold higher risk of recurrent seizures MRI scan mesial temporal sclerosis with temporal lobectomy for intractable epilepsy have 65-75% seizure free for up to 10 years post.

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3
Q

A patient has a complex partial seizures with normal neurological examination. What is the most likely etiology?

A

With a complex partial seizures with a normal examination, the most likely etiology is mesial temporal sclerosis.

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4
Q

What are some of the features of psychogenic seizures? What is the best step to investigate suspected psychogenic seizures?

A

(table from up to date) Psychogenic seizures usually: - last longer than 2 minutes - eyes closed (forced close suggests PNES) - forward pelvic thrusting, back arching (opisthotonus), rolling side to side, - activity waxes and wains, is irregular and asynchronous - vocalisation may occur - stuttering, weeping - incontinence less common - autonomic signs less common - may rapidly awaken and reorientate - headache rare The diagnostic procedure that is most likely to be beneficial in differentiating between epilepsy and psychogenic seizures is capturing an episode during video-EEG monitoring

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5
Q

What are the features of juvenile myoclonic epilepsy?

A
  • JME is a generalized epilepsy that typically presents during adolescence or early adulthood. - Patients typically describe a history of morning myoclonic jerks, and generalized seizures. Absence seizures are present in 20 - 40 % beginning up to five years before other seizure types. - Both seizures and the myoclonic jerks commonly are precipitated by sleep deprivation and alcohol. - The classic interictal electroencephalography (EEG) pattern in JME is 4 to 6 Hz bilateral polyspike and slow wave discharges with frontal predominance over a normal background activity. Sensitivity of the EEG rises to nearly 100 percent with overnight recording.
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6
Q

What should be quickly excluded in status?

A

hypoglycemia. If serum glucose is not immediately available, 50 cc of 50% dextrose should be administered intravenously concurrently with 100 mg of intravenous thiamine

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7
Q

What are the features of frontal lobe epilepsy?

A

Frontal lobe seizures can be diverse. They are commonly nocturnal and have prominent motor manifestations and automatisms. There may be no postictal confusion.” Common characteristics: - short duration - predilection to occur during sleep - seizure clusters and status epilepticus are more common than with TLE - post ictal state may be brief or absent Types: Focal seizures with impairment of consciousness - hypermotor behaviors (proximal limbs, tonic) - often bizarre looking - bicycling, automatisms (pelvic thrusting and sexual automatisms) - Tonic posturing and head and eye deviation (version), usually contralateral to the side of the seizure focus, - Vocalizations are also very common. seizure auras - common but less ubiquitous than TLE, ill described feeling, fear and anxiety Focal motor seizures involving the primary motor cortex will produce hemiclonic activity in the contralateral face, arm, or leg. Seizures may be quite focal (isolated to one limb or face) or may spread (or march) to adjacent areas (ie, Jacksonian seizure). Supplementary motor area seizures typically produce stereotyped asymmetric tonic movements. - fencing posture, (head deviates contralaterally) Speech arrest may accompany seizures arising from the dominant hemisphere. So-called frontal absence seizures manifest with staring, trance-like states.

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8
Q

What are the most common causes of seizures by decade?

A

Trauma in 2nd and 3rd decades Brain tumours in 4th decade Stroke in the elderly. - Acute cerebrovascular disease (including hemorrhagic and ischemic events) accounts for 60% of all cases of status epilepticus (SE) in the elderly.

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9
Q

Where to gustatory hallucinations typically arise from?

A

usually arising from a lesion of the parietal operculum.

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10
Q

After a first seizure - what factors increase risk of another?

A

After a first unprovoked seizure approx 1/3 will have a recurrent seizure in 5 years. The risk is higher if (2-2.5 fold higher) - Epileptiform abnormalities on interictal EEG - Remote symptomatic cause, as identified by clinical history or neuroimaging (eg, brain tumor, brain malformation, prior central nervous system infection) - Abnormal neurologic examination, including focal findings and intellectual disability - A first seizure that occurs during sleep With the above, risk approaches or exceeds 60% over 10 years, thereby meeting criteria for epilepsy according to the current International League Against Epilepsy (ILAE) definition.

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11
Q

What is SUDEP? What are the RFs for it?

A

Sudden unexplained death in epilepsy (SUDEP). Remains poorly understood. Most significant risk factors include 1. - uncontrolled generalized tonic-clonic convulsions - higher frequency of seizures - the need for multiple AEDs. - poor medical compliance - use of carbamazepine - mentally handicapped Absence seizures, nonconvulsive seizures, and etiology of the epilepsy, have no known bearing on the risk of SUDEP.

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12
Q

How do you manage drug resistant epilepsy?

A

Most patients who will respond to medical therapy will do so with the initial anticonvulsant. Medically refractory epilepsy. - traditionally failure of 3 AEDs = medically refractory epilepsy- although evidence that if fail 2 = medically refractory. In a patient who has failed to achieve good seizure control with monotherapy of two appropriate AEDs, or a combination of 2 drugs, the likelihood of response to a third drug is only 5% to 10%. After a trial of 2 x AED patients should be evaluated for alternative forms of therapy, including epilepsy surgery.

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13
Q

How can you monitor an intubated, sedated patient for status? (without EEG)

A

Intubation and general anesthesia interfere with observation of further seizure activity. pupillary dilatation and hypertension can be signs of ongoing seizure activity. Hypotension, poikilothermia (inability to regulate temp) and hypoventilation are likely secondary to sedative and anesthetic agents.

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14
Q

What is the definition of a late post-traumatic seizure?

A

“A late posttraumatic seizure is defined as a seizure that occurs more than 1 week after a head injury. Patients with a late posttraumatic seizure are at high risk for recurrent episodes and require long-term treatment with an AED, even after presentation of their first seizure.

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15
Q

Is prolactin level helpful for differentiating pseudoseizures?

A

For the assessment of true seizure versus pseudoseizure, EEG is indicated in the peri-ictal evaluation. Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic–clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children. However, the use of serum prolactin assay has not been established in the evaluation of status epilepticus, repetitive seizures, and neonatal seizures.”

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16
Q

What is fencer’s pose?

A

The fencer’s posture is associated with frontal lobe epilepsy and indicates epileptic activation of the supplemental motor area. It is described as external rotation and abduction of the contralateral arm from the shoulder, with head turning toward the same side of the arm posture.

17
Q

What are the characteristics of parietal lobe seizures?

A

Parietal lobe seizures are predominantly associated with episodic sensory symptoms, although clinical localization may be difficult as parietal discharges propagate to other brain regions. Parietal seizures are predominantly associated with episodic sensory symptoms, which include positive symptoms such as tingling or, less commonly, negative symptoms such as asomatognosia. In posterior parietal seizures, visual phenomena may occur.

18
Q

What are the characteristics of occipital lobe seizures?

A

Occipital lobe seizures usually present with visual phenomena.

19
Q

What are infantile spasms?

A

nfantile spasms occur during the first year of life (typically 3 to 8 months) and are discussed further in question 45. They are characterized by sudden tonic extension or flexion of limbs and axial body, often occurring in clusters, and especially shortly after awakening. Every patient presenting with infantile spasms should have an appropriate, thorough workup to look for the cause, including brain magnetic resonance imaging (MRI). In close to 30% of the cases, no specific etiology is found, and these cases are considered cryptogenic. Infantile spasms are frequent in patients with tuberous sclerosis, and this condition should be considered in this setting. West’s syndrome is a triad of infantile spasms, hypsarrhythmia, and psychomotor arrest or regression. This disorder often occurs because of pre/peri/postnatal insults, tuberous sclerosis, cerebral dysgenesis, and others. Treatment with ACTH is generally first line. Other treatments include corticosteroids, vigabatrin, clonazepam, levetiracetam, topiramate, pyridoxine, and valproic acid. Vigabatrin has been associated with retinal toxicity.

20
Q

Where is the lesion? (head turning and eye deviation to one side, then subsequent generalisation?

A

Eyes and head version, characterized strictly by a forced and involuntary movement leading to an unnatural position of the head toward one side, are associated with a seizure focus in the contralateral hemisphere and more specifically in the frontal region in the frontal eye fields and motor areas anterior to the precentral gyrus. The association of version with the contralateral hemisphere is more robust if the version occurs immediately prior to the secondarily GTC phase.

21
Q

What is the figure of four sign and where is the seizure starting?

A

Asymmetric tonic posturing in which his right arm is extended at the elbow with the fist clenched, while the left arm is flexed at the elbow. He subsequently has GTC seizures. This specific case describes the “figure of 4 sign,” in which the extended arm is contralateral to the seizure focus. Comes from contralateral supplementary motor area frontal lobe.

22
Q

Unilateral dystonic hand posturing with automatisms in other arm - Where is the epileptic focus?

A

temporal lobe ipsilateral to the automatisms Unilateral dystonic hand/arm posture during a seizure has important lateralizing value in temporal lobe epilepsies, suggesting that the seizure arises from the temporal lobe contralateral to the dystonic upper extremity. The suggested hypothesis is that the discharges originate in the hippocampus and the amygdala, spreading via the fornix and through the basal ganglia, more specifically the ventral striatum, pallidum, and anterior cingulate gyrus. Patients with dystonic posture of one upper limb and automatisms in the opposite upper limb have seizures originating in the temporal lobe ipsilateral to the automatisms.

23
Q

Seizure characterised by uncontrollable laughing - where is the lesions?

A

Gelastic seizures are characterized by uncontrollable episodes of laughter that occur in clusters, hese seizures are rare, and commonly originate in the hypothalamus, more specifically associated with hypothalamic hamartomas, although gelastic seizures arising from various cortical areas mainly in the frontal and temporal lobe have been well described in the literature. Hypothalamic hamartoma is a congenital malformation that may be asymptomatic in some cases but commonly presents with precocious puberty and seizures

24
Q

What investigations have good evidence after first unprovoked seizure?

A

According to practice parameter guidelines published by the American Academy of Neurology, there is good evidence to support both the use of a routine EEG and brain imaging with CT or MRI in patients presenting with a first unprovoked seizure. There is inadequate evidence to support or refute laboratory studies, lumbar puncture, and toxicology screens. However, specific clinical circumstances may support the need for these additional tests on an individual basis, such as if the patient is febrile and CNS infection is suspected, in which case a lumbar puncture would be diagnostic.

25
Q

After a first unprovoked seizure-when is the risk highest for another?

A

Not every patient with a first unprovoked seizure needs to be treated. According to the same 2015 guidelines, there is strong evidence that seizure recurrence is greatest in the first 2 years after a first seizure (21% to 45%).

26
Q

immediate vs delayed AED initiation after first seizure?

A

Immediate AED therapy as compared with the delay of treatment pending a second seizure is likely to reduce seizure recurrence in the subsequent 2 years, but it may not improve quality of life. Furthermore, over the longer term (>3 years), immediate AED therapy is unlikely to improve the prognosis for sustained seizure remission. The risk of AED adverse effects ranges from 7% to 31%, but they are predominantly mild and reversible.

27
Q

What is the diagnosis of OSA?

A

Obstructive sleep apnea (OSA) is diagnosed on the basis of a combination of clinical features (discussed in question 87) and the apnea-hypopnea index (AHI) observed during an overnight polysomnogram. Apneas and hypopneas are characterized by complete cessation or reduction of airflow, respectively, for at least 10 seconds. In addition, obstructive hypopneas/apneas are associated with EEG arousal and/or oxygen desaturation (of 3% to 4%, depending on the criteria being employed). The AHI is a measure of how many apneas and hypopneas, on average, occur per hour. An AHI of 5 to 15 per hour is considered mildly elevated, of 15 to 30 per hour moderately elevated, and more than 30 per hour is severely elevated. A similar index of apneas and hypopneas is the so-called respiratory disturbance index, which in addition to apneas and hypopneas also accounts for respiratory-event-related arousals.

28
Q

What are sleep terrors?

A

This patient has a non-REM parasomnia, more specifically sleep terrors. Parasomnias have been classified into REM parasomnias, arousal disorders, sleep–wake transition disorders, and other parasomnias. Arousal disorders include confusional arousals, sleepwalking, and sleep terrors. The latter three are non-REM parasomnias typically arising from slow-wave sleep or stage N3 (previously known as stage 3 and stage 4 sleep; these two stages have been combined into stage N3). Sleep terrors are more common in children, usually occurring between the ages of 5 and 7 years but can occur in adults. These events are characterized by a sudden arousal with screaming or crying, associated with autonomic and behavioral manifestations of intense fear and some degree of confusion if awakened. Sleep terrors occur in the first third of the night (a period during which stage N3 is most likely to occur). In nightmares, as opposed to sleep terrors, the patients usually remember the dream, they occur in the last third of the night, and there is less autonomic activity.

29
Q

Explain sleepwalking?

A

Sleep walking is a non-REM parasomnia. Parasomnias have been classified into REM parasomnias, arousal disorders, sleep–wake transition disorders, and other parasomnias. Arousal disorders include confusional arousals, sleepwalking, and sleep terrors. The latter three are non-REM parasomnias arising from slow-wave sleep or stage 3 sleep (previously known as stage 3 and stage 4 sleep; these two stages have more recently been combined into stage 3 sleep). Sleepwalking consists of a series of complex behaviors resulting in walking during sleep. This condition occurs more commonly in children but can present in adolescents and adults, and a positive family history has been reported in many cases. Sleepwalking occurs more commonly in the first third of the night, and patients have complex motor behaviors, with amnesia of the episode. These patients are difficult to arouse and may become confused and exhibit violent behavior when this is attempted.

30
Q

What does this sleep study show? What disease is likely to develop?

A

This patient has a REM parasomnia, specifically REM sleep behavior disorder (RBD).

Normally, there is atonia (loss of muscle tone) during REM sleep. RBD is characterized by at least intermittent loss of this normal REM atonia as is shown in Figure 5.14B (blue arrow) and by the appearance of complex motor activity during which the patient acts out dreams. Dream content is usually violent with associated movements (e.g., punching, kicking, and running). This can cause injuries to the patient or to the bed partner. The prevalence of RBD increases with increasing age. Over half of patients with RBD go on to develop a neurodegenerative disorder, most often α-synucleinopathies such as Parkinson’s disease, multisystem atrophy, or dementia with Lewy bodies. Of all the disorders listed in question 92, only Parkinson’s disease is an α- synucleopathy. Treatment of RBD includes interventions to minimize risk of injury (such as padding the headboard and bedside table) as well as pharmacologic agents such as melatonin and clonazepam.

31
Q

What is Kleine-Levin Syndrome

A

This patient has Kleine–Levin syndrome, which is a type of recurrent hypersomnia. This condition is characterized by recurrent episodes of hypersomnia that typically occur weeks or months apart. Onset is in early adolescence and the episodes can last for several days and sometimes weeks, appearing many times per year. Patients sleep for prolonged periods of time, 18 to 20 hours, often waking only to eat and void. During these episodes, patients may exhibit irritability, aggressiveness, confusion, hypersexuality, and a voracious appetite. Disturbance of social life is significant during these episodes. In between episodes, patients sleep normal amounts and behave normally. This disorder is more common in males but can occur in females, in whom episodes of hypersomnolence may occur around the time of menstruation.

32
Q

What is idiopathic hypersomnia?

A

Idiopathic hypersomnia is characterized by chronic excessive daytime sleepiness, in the absence of a primary nocturnal sleep disorder, or other medical condition or factor that could account for the hypersomnolence. Patients complain of hypersomnia and sleep for long periods of time, but the sleep is not refreshing. The diagnosis is made only when no other medical or psychiatric condition can explain the hypersomnia.

33
Q

What is narcolepsy?

A

Narcolepsy in its classic form, now called type 1 narcolepsy, is a disorder that is characterized by excessive sleepiness, cataplexy, sleep paralysis, and hypnagogic and hypnopompic hallucinations. Patients with narcolepsy suffer sleep attacks, with episodes of involuntary sleep in inappropriate circumstances. Brief episodes of sleep, or volitional naps, lasting 15 to 30 minutes are usually refreshing.

34
Q

What is sleep paralysis?

A

Sleep paralysis is characterized by persistence of REM atonia in wakefulness. Clinically, it is characterized by a transient paralysis during sleep onset or on awakening; the patient is fully conscious during these events. Sleep paralysis is a feature of narcolepsy (discu

35
Q

How does narcolepsy with cataplexy present?

A

This patient has narcolepsy with cataplexy, now called type 1 narcolepsy. This is a disorder characterized by excessive sleepiness, cataplexy, sleep paralysis, and hypnagogic and hypnopompic hallucinations (discussed in question 93). Patients with narcolepsy suffer sleep attacks, in which the patient has an irresistible desire to fall asleep during inappropriate circumstances. These sleep attacks are short, lasting 15 to 30 minutes, and the patient feels refreshed afterward. Although cataplexy is associated with narcolepsy, not all patients with narcolepsy have cataplexy. Cataplexy is characterized by episodes of sudden loss of tone of voluntary muscles, sparing respiratory and ocular muscles. During these attacks, remove the patients may fall and be unable to move, and deep tendon reflexes are decreased or absent. Patients have preserved consciousness.

Cataplectic attacks may be triggered by emotional events, such as laughter or anger. The diagnosis of narcolepsy is supported by two features on a daytime multiple sleep latency test: (i) a mean sleep latency of 8 minutes or less and (ii) REM sleep within 15 minutes of sleep onset, during at least two of four nap trials.

Cataplexy may be misdiagnosed as seizures, pseudoseizures, or conversion disorder/psychogenic events. However, the triggering of episodes by emotion as well as other features including hypersomnolence should prompt consideration of narcolepsy. Sleep paralysis, transient paralysis that intrudes from REM sleep into wakefulness, is also commonly associated with narcolepsy (discussed in question 93).

Gamma-hydroxybutyrate has been approved for the treatment of sleepiness and cataplexy in the United States. Other treatment options for cataplexy include tricyclic antidepressants or serotonin reuptake inhibitors.