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Paroxysmal attack
Paroxysmal attack
Paroxysmal attack
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Paroxysmal attack
Other namesParoxysms
SpecialtyNeurology Edit this on Wikidata

Paroxysmal attacks or paroxysms are a sudden recurrence or intensification of symptoms, such as a spasm or seizure.[1] These short, frequent symptoms can be observed in various clinical conditions. They are usually associated with multiple sclerosis or pertussis, but they may also be observed in other disorders such as encephalitis, head trauma, stroke, autism, asthma, trigeminal neuralgia, breath-holding spells, epilepsy, malaria, tabes dorsalis, Behçet's disease, and paroxysmal nocturnal hemoglobinuria (PNH). It has also been noted as a symptom of gratification disorder in children.[citation needed]

The word paroxysm means 'sudden attack, outburst'[2] and comes from Greek παροξυσμός (paroxusmós) 'irritation, exasperation'.[3]

Paroxysmal attacks in various disorders have been reported extensively, and ephaptic coupling of demyelinated nerves has been presumed as one of the underlying mechanisms of this phenomenon. This is supported by the presence of these attacks in multiple sclerosis and tabes dorsalis, which both involve demyelination of spinal cord neurons. Exercise, tactile stimuli, hot water, anxiety, and neck flexion may provoke paroxysmal attacks. Most reported paroxysmal attacks are painful tonic spasms, dysarthria and ataxia, numbness, and hemiparesis. They are typically different from other transient symptoms by their brevity (lasting no more than 2 minutes), frequency (from 1–2 times/day up to a few hundred times/day), stereotyped fashion, and excellent response to drugs (usually carbamazepine). Withdrawal of symptoms without any residual neurological finding is another key feature in their recognition.[citation needed]

See also

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References

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Paroxysmal attack

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A paroxysmal attack, also known as a paroxysm, is a sudden and often violent episode of symptoms in a medical condition, characterized by the abrupt onset, intensification, or recurrence of manifestations such as , spasms, convulsions, or other disturbances, typically lasting from a few seconds to several minutes before resolving spontaneously. This term derives from word "paroxysmós," meaning or exasperation, and emphasizes the episodic, self-limited nature of the event, distinguishing it from chronic or progressive symptoms. Paroxysmal attacks occur across various medical fields. In neurology, they are a hallmark of episodic disorders arising from transient disruptions in neural activity, with common examples including epileptic seizures, paroxysmal symptoms in such as sensory disturbances or tonic spasms, and paroxysmal like kinesigenic dyskinesias. In cardiology, they manifest as paroxysmal , involving sudden episodes of irregular heartbeat that resolve spontaneously within seven days. Other examples include paroxysmal nocturnal dyspnea in respiratory or cardiac conditions, characterized by sudden at night.

Overview

Definition

A paroxysmal attack is defined as a sudden, discrete of symptoms that begins abruptly, escalates to peak intensity rapidly, and resolves spontaneously or with minimal intervention, typically enduring from seconds to minutes, though durations up to hours may occur in certain cases. This distinguishes paroxysmal attacks from continuous or progressive symptoms in chronic disorders, where manifestations persist without clear onset and resolution phases, emphasizing instead the self-limited and recurrent episodic pattern. The term originates from the Greek paroxysmos, meaning "irritation" or "exasperation," derived from para- (beside or during) and oxys (sharp or acute), evoking the sharp, aggravating onset of such episodes. It entered medical literature in the 15th century to denote sudden fits or exacerbations, particularly in describing episodic worsenings of diseases like fevers or convulsions.

Characteristics

Paroxysmal attacks are distinguished by their abrupt onset, often occurring without any preceding warning or , which sets them apart from more gradual symptom progressions in other disorders. These episodes typically escalate rapidly to peak intensity within seconds to minutes, reflecting a sudden dysregulation in the affected physiological system. The short duration of attacks, generally ranging from seconds to minutes though up to several hours in some cases, underscores their transient nature, with most resolving spontaneously without intervention. A defining feature is the stereotyped recurrence of episodes, where subsequent attacks in an individual exhibit consistent patterns of symptoms, duration, and manifestations, facilitating recognition once identified. Full interictal recovery is another key trait, with patients returning to their normal baseline function between episodes, devoid of persistent neurological or physiological deficits. Potential triggers, such as sudden movement or emotional stress, may precipitate attacks in some cases, though many occur unprovoked. The frequency of paroxysmal attacks varies considerably across individuals and conditions, potentially manifesting daily, weekly, or at irregular intervals; episodes may cluster during periods of heightened vulnerability or enter phases of remission over time. Symptom intensity during an attack builds swiftly to maximum severity, often rendering the experience profoundly debilitating—such as through intense pain, motor disruption, or autonomic instability—despite the brevity of the event, which can significantly impair . These characteristics are exemplified in paroxysmal symptoms linked to underlying conditions like .

Pathophysiology

Mechanisms

In neurological paroxysmal attacks, these episodes arise from hyperexcitability within neuronal networks, where an imbalance in excitatory and inhibitory influences promotes synchronized firing of neurons, leading to abrupt episodes of abnormal electrical activity. This hyperexcitability often stems from dysfunction in ion channels, particularly voltage-gated sodium and calcium channels, which destabilize neuronal membranes by altering the threshold for action potential generation and propagation. Such channelopathies can result from genetic mutations that impair normal ion flux, though these are explored further in discussions of etiology. A key contributor to this process is the imbalance between excitatory and inhibitory , where excessive glutamate signaling enhances neuronal activation while diminished GABA-mediated inhibition fails to counteract it, thereby initiating cascading excitatory events. This dysregulation amplifies network excitability, transforming localized disturbances into widespread paroxysmal discharges. Once initiated, these attacks involve self-propagating feedback loops of electrical activity, where synchronized neuronal firing reinforces itself through recurrent synaptic connections, sustaining the episode until termination occurs via neuronal exhaustion—depletion of energy stores and neurotransmitters—or through compensatory inhibitory mechanisms that restore balance.

Etiology

Paroxysmal attacks arise from a combination of primary etiologies, including genetic predispositions, acquired factors, and idiopathic origins. Genetic factors often involve channelopathies, where mutations in genes disrupt neuronal excitability; for instance, mutations in the PRRT2 gene are a leading cause of paroxysmal kinesigenic and related disorders, leading to recurrent episodes through impaired synaptic transmission. Acquired etiologies typically stem from brain lesions resulting from trauma, such as , or infections like , which can precipitate paroxysmal sympathetic hyperactivity by damaging regulatory centers in the and . In many cases, particularly within syndromes, paroxysmal attacks occur without identifiable structural or genetic causes, classified as idiopathic and potentially linked to subtle developmental abnormalities. Risk factors for paroxysmal attacks encompass demographic, hereditary, medical, and environmental elements that increase susceptibility. Age plays a significant role, with higher incidence in young adults for certain genetic forms like PRRT2-related disorders and in older individuals for acquired cases tied to cerebrovascular events. history elevates risk, as autosomal dominant patterns are common in channelopathies, with up to 80% of affected families showing PRRT2 variants. Comorbidities such as contribute to vascular instability that may trigger cardiovascular paroxysmal events, while coexisting heightens the likelihood of recurrent neurological attacks. Environmental triggers, including , can lower the and provoke episodes by altering cortical excitability. These etiologies contribute to paroxysmal attacks by inducing neuronal or systemic instability through distinct pathogenic pathways. Genetic mutations, such as those in PRRT2, lead to synaptic dysfunction that destabilizes membrane potentials, often involving involvement as detailed in pathophysiological mechanisms. Acquired lesions from trauma or disrupt neural circuits, creating foci of hyperexcitability that propagate sudden discharges. , arising from infectious or post-traumatic processes, further exacerbates this by releasing cytokines that lower the threshold for neuronal firing, thereby facilitating recurrent attacks.

Classification and Types

Neurological Paroxysmal Attacks

Neurological paroxysmal attacks encompass episodic disorders primarily involving the central or , manifesting as sudden, transient disruptions in motor, sensory, or autonomic function, which may or may not involve loss of consciousness. These attacks are characterized by their brevity and stereotyped nature, often triggered by specific stimuli, and can mimic epileptic seizures or other acute neurological events. Key examples include epileptic seizures, paroxysmal kinesigenic dyskinesia (PKD), paroxysmal hemicrania, and paroxysmal tonic spasms in (MS), each presenting with distinct neurological symptoms such as altered consciousness or convulsions, involuntary movements, severe headaches, or sensory-motor bursts. Epileptic seizures are a primary example of neurological paroxysmal attacks, characterized by hypersynchronous neuronal firing leading to sudden episodes of altered , convulsions, or focal motor activity, often lasting seconds to minutes. Paroxysmal kinesigenic represents one of the most common paroxysmal , featuring recurrent attacks of dystonic or choreoathetotic movements provoked by sudden voluntary movements or startle. These episodes typically last less than one minute, involve brief, involuntary twisting or flinging motions of the limbs, and spare , with patients often experiencing a sensory aura preceding the attack. The prevalence of PKD is estimated at 1 in 150,000 individuals, predominantly affecting those of Asian descent, though it can occur worldwide. relies on clinical history, as interictal electroencephalogram (EEG) findings are usually normal, but video-EEG monitoring during provoked attacks may reveal no epileptiform activity, helping differentiate it from seizure-like events. Paroxysmal hemicrania is a rare trigeminal autonomic cephalalgia marked by severe, unilateral orbital, supraorbital, or temporal pain described as sharp or stabbing, accompanied by ipsilateral autonomic features such as lacrimation, , or ptosis. Attacks endure 2 to 30 minutes and occur more than five times daily, up to 40 episodes in severe cases, often causing restlessness or agitation during bouts. Its prevalence remains poorly defined but is estimated at a relative frequency of 0.3% among patients evaluated for headaches in specialized clinics. Diagnostic evaluation includes EEG if mimicry is suspected, though abnormalities are uncommon; instead, absolute response to indomethacin serves as a key confirmatory clue, alongside to exclude secondary causes. In , paroxysmal symptoms like tonic spasms arise from demyelination-induced ephaptic transmission, presenting as sudden, stereotyped episodes of muscle stiffness or painful contractions, often affecting the limbs or trunk and lasting seconds to minutes. These spasms can occur 10 to 20 times daily or more, sometimes triggered by movement or , and may include sensory bursts such as or , alongside rarer vertigo-like episodes. Such symptoms affect 1.6% to 17% of MS patients over the disease course, with paroxysmal manifestations as the initial presentation in approximately 0.77% to 1.1% of cases. EEG during attacks typically shows no epileptiform discharges in these non-epileptic events, aiding differentiation from true seizures through normal findings or lack of ictal changes.

Cardiovascular Paroxysmal Attacks

Cardiovascular paroxysmal attacks refer to sudden, transient disruptions in cardiac rhythm or function, primarily manifesting as arrhythmias that onset and terminate abruptly, often without permanent damage if managed appropriately. These episodes are characterized by irregular or rapid heartbeats originating above the ventricles, distinguishing them from sustained or ventricular arrhythmias. Common in adults over 50, they can occur in structurally normal hearts or alongside conditions like , which increases susceptibility through atrial remodeling. A primary example is paroxysmal atrial fibrillation (PAF), defined as recurrent episodes of irregular atrial activity lasting less than seven days that spontaneously revert to normal . In PAF, the atria quiver ineffectively due to disorganized electrical impulses, leading to an irregular ventricular response. Symptoms typically include , , and , which may resolve as the episode ends, though some patients experience or during attacks. Approximately 20-30% of all cases present as paroxysmal, making it a frequent initial manifestation in newly diagnosed patients. The electrophysiological basis of PAF involves re-entrant circuits within the atria or ectopic foci, often originating from pulmonary veins, that initiate and sustain the through rapid, uncoordinated firing. These foci generate premature beats that propagate chaotically, while re-entry exploits heterogeneous conduction properties to create self-perpetuating loops. Another key example is (PSVT), particularly atrioventricular nodal re-entrant tachycardia (AVNRT), where a dual pathway in the AV node allows re-entrant impulses to cycle rapidly, producing a sudden exceeding 150 beats per minute. PSVT symptoms mirror those of PAF, including , , and , with a of about 2.25 per 1,000 individuals.

Other Paroxysmal Attacks

Benign paroxysmal positional vertigo (BPPV) represents a common vestibular paroxysmal attack characterized by brief episodes of or vertigo triggered by specific changes in head position, such as rolling over in bed or looking upward. The underlying mechanism involves the displacement of otoconia— crystals from the utricle—into one of the , where they stimulate hair cells during head movements, producing and the sensation of spinning. These attacks are typically self-limited, lasting seconds to minutes, and are position-specific, distinguishing them from continuous vestibular disorders. The lifetime prevalence of BPPV is approximately 2.4%, with higher rates in women and individuals over 50 years old. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired hematologic disorder manifesting as episodic intravascular , often occurring at night or upon awakening, leading to dark urine due to release. This condition arises from a in the in hematopoietic stem cells, resulting in deficient (GPI) anchor synthesis, which renders red blood cells susceptible to complement-mediated . Attacks are intermittent and can be exacerbated by factors like infections, , or , presenting with , , and alongside the hemolytic episodes. PNH affects approximately 1-2 per million individuals annually, with episodes varying in frequency and severity among patients. Paroxysmal cold hemoglobinuria (PCH), a rare form of , involves acute episodes of triggered by exposure to cold temperatures, often following viral infections in children or as an idiopathic process in adults. The mechanism centers on the biphasic Donath-Landsteiner antibody, an IgG that binds to (typically P antigen) at temperatures below 4°C, fixes complement, and induces upon rewarming to body temperature. Symptoms include sudden , , and during or after cold exposure, with episodes resolving spontaneously but potentially recurring with repeated triggers. PCH is exceedingly uncommon, comprising less than 1% of autoimmune hemolytic anemias, and is often self-limited in post-infectious cases.

Diagnosis

Clinical Evaluation

The clinical evaluation of paroxysmal attacks begins with a thorough history-taking to characterize the episodic nature of the symptoms, which is essential for initial classification and guiding further investigation. Patients are encouraged to maintain a detailed attack diary documenting the precise onset, duration (often seconds to minutes for neurological events or longer for cardiovascular ones), associated triggers (e.g., sudden movement, stress, or posture changes), and any prodromal symptoms such as auras, , or . This approach helps identify patterns, such as stereotyped recurrences, and distinguishes true paroxysmal events from continuous or progressive disorders. Family history is systematically explored to uncover hereditary patterns, as many paroxysmal attacks, particularly neurological types like paroxysmal kinesigenic dyskinesia, have genetic underpinnings, while cardiovascular variants may link to familial arrhythmias. Comorbidities, including , diabetes, psychiatric conditions, or substance use, are assessed, as they can precipitate or exacerbate episodes and influence the differential. Witness accounts are invaluable, providing objective details on observable features like loss of consciousness or involuntary movements that the patient may not recall. The focuses on identifying subtle clues during or immediately after an episode, though interictal exams are often normal. For neurological paroxysmal attacks, a comprehensive assessment checks for focal deficits, such as unilateral weakness, sensory changes, or gait abnormalities, alongside cranial nerve function and mental status. Cardiovascular evaluation includes monitoring for pulse irregularity or , auscultation for murmurs or bruits, and orthostatic testing to detect triggers like vasovagal responses. These findings help localize potential etiologies and rule out acute complications. Differential diagnosis relies on symptom clustering to exclude mimics, emphasizing the abrupt, focal, and self-limited quality of paroxysmal attacks. For instance, neurological features like unilateral motor deficits favor ischemic events over the bilateral, gradual symptoms of migraines (e.g., with ) or the and associated with panic attacks. This , combined with absence of post-event confusion in non-epileptic cases, refines the assessment without immediate reliance on or labs. Common cardiovascular examples, such as paroxysmal , may present with but lack focal neurology, aiding distinction.

Diagnostic Tests

Diagnostic tests for paroxysmal attacks aim to capture episodic events, rule out structural abnormalities, and identify underlying etiologies through objective measures such as , , and genetic . Selection of tests is guided by the suspected type of attack, with neurological paroxysmal events often requiring (EEG) to detect ictal activity, while cardiovascular episodes necessitate cardiac rhythm monitoring. For neurological paroxysmal attacks, such as paroxysmal kinesigenic dyskinesia or episodic ataxias, video-EEG monitoring is a diagnostic tool, allowing simultaneous capture of clinical symptoms and electrical activity to differentiate epileptic from non-epileptic events. Interictal EEG is frequently normal in these disorders, but prolonged video-EEG (up to several days) increases the yield for documenting ictal changes during attacks. MRI is routinely performed to exclude structural lesions like tumors or vascular malformations that could trigger attacks, though it is often normal in primary or idiopathic paroxysmal . In cardiovascular paroxysmal attacks, such as paroxysmal atrial fibrillation (AFib) or arrhythmias causing syncope, ambulatory ECG monitoring via Holter devices or event recorders is essential for detecting intermittent rhythm disturbances. A 24-hour Holter monitor identifies paroxysmal AFib in about 1-5% of cryptogenic stroke patients, though extending to 7-day monitoring boosts the detection rate to around 5-10%. For syncope-like attacks, tilt-table testing reproduces orthostatic stress to provoke vasovagal or orthostatic hypotension responses, with a diagnostic yield of around 50% in unexplained syncope cases when combined with pharmacological provocation like nitroglycerin. Advanced diagnostic methods include for channelopathies underlying certain paroxysmal attacks, such as sequencing the PRRT2 gene in suspected paroxysmal kinesigenic dyskinesia, where mutations are identified in 70-80% of familial cases and guide confirmatory when clinical features and normal EEG/MRI align. Implantable loop recorders provide long-term monitoring (up to years) for rare recurrent events, offering higher sensitivity than external devices for elusive paroxysmal arrhythmias. Interpretation of these tests emphasizes correlating findings with clinical , as false negatives are common due to the transient nature of attacks, necessitating repeat or prolonged monitoring for optimal yield.

Management and Treatment

General Principles

The management of paroxysmal attacks begins with acute stabilization to ensure during episodes, following the established ABC approach of assessing and securing the airway, supporting , and maintaining circulation, which is applicable across clinical emergencies including sudden paroxysmal events. This initial response prioritizes preventing hemodynamic instability or loss of consciousness, with immediate avoidance of identified triggers—such as sudden movements in certain neurological subtypes—to terminate or mitigate the attack. Lifestyle modifications form a foundational for reducing the frequency and severity of paroxysmal attacks, emphasizing through consistent routines to minimize fatigue-related triggers, stress reduction techniques like or relaxation exercises, and adequate hydration to support physiological stability. For cardiovascular variants, prophylactic measures include limiting alcohol intake, as excessive consumption can precipitate episodes by altering cardiac rhythm. Patient education is integral, empowering individuals to recognize early symptoms of impending attacks and implement safety protocols, such as avoiding or operating machinery during high-risk periods to prevent accidents. This involves maintaining a symptom to track patterns and triggers, fostering self-management and timely seeking of medical help. A multidisciplinary approach coordinates care among specialists tailored to the underlying type, such as neurologists for movement-related attacks or cardiologists for rhythm disturbances, alongside providers to integrate holistic monitoring and preventive strategies.

Specific Therapies

Specific therapies for paroxysmal attacks are tailored to the underlying , with treatments targeting neurological, cardiovascular, and other manifestations to interrupt or prevent recurrent episodes. In neurological paroxysmal attacks, such as paroxysmal kinesigenic dyskinesia (PKD), anticonvulsants like are first-line agents due to their blockade of sodium channels, yielding response rates exceeding 80% in reducing attack frequency and severity. serves as an alternative with similar efficacy to carbamazepine. For paroxysmal hemicrania, a trigeminal autonomic cephalalgia, indomethacin acts both diagnostically and therapeutically by inhibiting synthesis, providing complete relief in nearly all responsive cases at doses of 25-150 mg daily, confirming the diagnosis when attacks cease. Cardiovascular paroxysmal attacks, including paroxysmal atrial fibrillation (AFib), often respond to beta-blockers such as metoprolol for rate control during episodes, reducing ventricular response and symptom burden in acute settings. Antiarrhythmics like , a class Ic agent, are preferred for rhythm control in structurally normal hearts, effectively preventing recurrences with good tolerability over 12 months in outpatient management. For recurrent (PSVT), targeting accessory pathways or slow pathways achieves acute success rates over 90%, with long-term cure in 95-98% of cases and low recurrence. Among other paroxysmal attacks, the addresses (BPPV) by repositioning displaced otoconia in the , resolving vertigo in 80-90% of patients after one or two sessions through canalith repositioning. In (MS)-related paroxysmal symptoms, such as tonic spasms or dyskinesias from demyelination, pulse corticosteroids like intravenous (1 g/day for 3-5 days) rapidly suppress ephaptic transmission, alleviating attacks in most cases as the primary intervention.

Prognosis and Complications

Outcomes

Paroxysmal attacks exhibit a variable depending on the underlying type, with many forms being benign and self-limiting, resolving spontaneously within weeks to months without long-term sequelae. For instance, (BPPV), a common vestibular paroxysmal disorder, often follows a self-limited course, with symptoms typically disappearing in weeks or months in untreated cases. In contrast, other paroxysmal conditions, such as paroxysmal (AFib), tend to be more chronic, though controllable with management; approximately 10-15% of cases progress annually to a persistent form, potentially increasing risks of if untreated. Several factors influence recovery and long-term outcomes in paroxysmal attacks. Early intervention, such as repositioning maneuvers for BPPV or rhythm control strategies for paroxysmal AFib, significantly improves by reducing recurrence and progression rates. Conversely, advanced age and comorbidities like , , or worsen outcomes, increasing the likelihood of recurrence and complicating resolution in disorders such as BPPV and paroxysmal AFib. Remission rates vary markedly between genetic and acquired paroxysmal attacks. Genetic forms, such as paroxysmal kinesigenic dyskinesia (PKD), often remit or improve during , with symptoms resolving in up to 50-60% of familial cases as frequency decreases with age. For acquired paroxysmal attacks, remission largely depends on addressing the underlying cause, such as metabolic imbalances or structural lesions, where targeted treatment can lead to complete resolution in responsive cases.

Associated Risks

Paroxysmal attacks carry acute risks primarily related to sudden loss of balance or consciousness, leading to falls and subsequent injuries. In conditions such as (BPPV), the intense dizziness can cause unsteadiness, increasing the likelihood of falls and potential trauma like fractures or head injuries. Similarly, during epileptic s, falls are a common consequence, heightening the risk of concussions, lacerations, and other , with higher seizure frequency correlating to greater injury incidence. In cardiovascular manifestations like paroxysmal (AF), acute risks include thromboembolic events, where the elevates risk by approximately fivefold compared to the general population. Chronic complications arise from recurrent or untreated episodes, potentially leading to disease progression and secondary effects. Paroxysmal AF often advances to persistent or permanent forms, with studies indicating that 10-20% of patients progress within one year, influenced by factors such as age and comorbidities. In movement disorders, paroxysmal dyskinesias may involve dystonic elements during attacks, and prolonged untreated recurrence can contribute to more sustained dystonic postures over time. Additionally, the unpredictable nature of these attacks fosters psychological distress, including heightened anxiety and depression, which can exacerbate attack frequency and duration in disorders like paroxysmal kinesigenic dyskinesia or BPPV. Mortality associated with paroxysmal attacks remains low in non-cardiac forms, such as episodic vertigo or dyskinesias, which are generally benign with minimal direct fatal outcomes. However, cardiac variants like paroxysmal confer elevated risks, with annual all-cause mortality rates around 7% and untreated incidence ranging from 1-2% in lower-risk patients, underscoring the need for anticoagulation to mitigate these dangers.

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