Prodrome - an overview | ScienceDirect Topics (2023)

Premonitory Symptoms, Aura, and Accompanying Symptoms

Some patients have premonitory symptoms that precede a migraine headache by hours. These can include psychological changes (e.g., depression, euphoria, irritability) or somatic symptoms (e.g., constipation, diarrhea, abnormal hunger, fluid retention, increased urination). The termaura refers to focal cerebral symptoms associated with a migraine attack. These symptoms can last 5–60 minutes but usually last 10–30 minutes. Aura symptoms typically precede the headache but can continue into the headache phase or begin during the headache. Visual symptoms are most common and may consist of either positive (scintillating lights, spots, or zig-zag lines) or negative (scotomas or visual field loss) phenomena or both. The visual symptoms characteristically affect both eyes simultaneously but can rarely affect one eye alone. Less common hemispheric symptoms, such as unilateral somatosensory disturbances (tingling and/or numbness) or dysphasic language disturbance, may occur with or without visual symptoms. Aura symptoms usually have a gradual onset and offset; they typically increase and decrease over minutes. If more than one symptom occurs (e.g., visual plus somatosensory), the onsets usually are staggered and not simultaneous. Patients can experience migraine aura without an associated headache. Positive symptoms, the slow spread of symptoms, and staggered onsets help differentiate migraine aura from focal symptoms caused by cerebrovascular disease.

Symptoms originating from the brainstem or both cerebral hemispheres simultaneously—such as vertigo, dysarthria, ataxia, auditory symptoms, diplopia, bilateral visual symptoms in both eyes, bilateral numbness and/or paresthesias, and decreased level of consciousness—may accompany migraine with brainstem aura (formerly called basilar-type migraine) (IHS, 2018). Vertigo without other brainstem signs can also accompany migraine headaches. Migraine with aura that includes motor weakness can be due to familial hemiplegic migraine if there is a family history in at least one first- or second-degree relative or due to sporadic hemiplegic migraine if there is no family history. It can be difficult for the patient to differentiate sensory loss from true weakness, but this must be carefully delineated. Nausea, vomiting, photophobia, phonophobia, and osmophobia characteristically accompany migraine attacks. In addition, lacrimation, rhinorrhea, and nasal congestion can accompany migraine headache and mimic headache of sinus origin (Cady etal., 2005). Ipsilateral miosis, ptosis, lacrimation, conjunctival injection, and nasal stuffiness commonly accompany cluster headache; sweating and facial flushing on the side of the pain are much less common. Similar autonomic features also accompany episodic and chronic paroxysmal hemicrania and hemicrania continua. Very short attacks (5–240 seconds) with ipsilateral conjunctival injection and tearing suggest SUNCT (Goadsby, 2012). Horner syndrome is common in carotid artery dissection. In the setting of acute transient or persistent monocular visual loss, GCA and carotid dissection and stenosis should be considered. Temporomandibular joint dysfunction includes jaw pain precipitated or aggravated by movement of the jaw or clenching of the teeth and is associated with reduced range of jaw movement, joint clicking, and tenderness over the joint. Headache accompanied by fever suggests an infection. Headache associated with persistent or progressive diffuse or focal central nervous system (CNS) symptoms, including seizures, implies a structural cause. Purulent or bloody nasal discharge suggests an acute sinus cause for the headache. Likewise, a red eye raises the possibility of an ocular process such as infection or acute glaucoma. A history of polymyalgia rheumatica, jaw claudication, or tenderness of the scalp arteries in an older person strongly suggests GCA. Transient visual obscurations upon standing, usually pulsatile tinnitus, diplopia (especially for objects in the distance), and papilledema may be associated with increased intracranial pressure from any cause, including idiopathic intracranial hypertension (pseudotumor cerebri).

History

Try to obtain a history from eye-witness as well as from the patient themselves.

History from the patient:

Context: may suggest likely cause – a collapse when having blood taken suggests syncope; an episode arising from sleep suggests a seizure.

Prodrome: a brief sensation of déjà vu before the episode indicates a focal onset seizure; a feeling of lightheadness, sweatiness and visual fading suggests syncope.

Recovery: a rapid recovery suggest syncope; waking in the ambulance suggest seizure.

History from witness (find them; phone them):

How long the patient was out for; – syncope is typically less than 1 minute; seizures usually longer.

What they did; brief asynchronous jerking movements occur in syncope; more prolonged synchronous tonic clonic movements occur in seizures.

Any colour change; ‘ashen’ suggests syncope; cyanosed suggests seizure.

How quickly they recovered; rapid recovery suggest syncope.

Silent witnesses:

Incontinence is common in all forms of loss of consciousness and does not distinguish between a seizure and syncope. Tongue biting strongly suggests a seizure as do other much less common injuries – posterior dislocation of the shoulder or vertebral fracture.

Investigation is directed by the clinical history:

Electroencephalography (EEG) may reveal a focal or generalized disturbance – epilepsy.

Electrocardiography (ECG) and 24 hour ECG may reveal a cardiac arrythmia.

Head up tilt-table testing may reveal neurocardiogenic syncope or orthostatic hypotension.

Echocardiography may reveal cardiomyopathy.

Blood glucose may indicate hypoglycaemia.

EEG telemetry is occassionally needed.

Often attacks of unconsciousness remain unexplained and possibly have a psychological basis. The circumstances of the attack (e.g. during an argument), the non-stereotyped nature of the episode suggest a non-organic explanation. Such attacks are often mistaken for a seizure and are referred to as pseudo-seizures or non-epileptic attacks (see page 99).

Prodromal Symptoms

The initial symptoms of rabies resemble those of other systemic viral infections, including fever, headache, malaise, and disorders of the upper respiratory and gastrointestinal (GI) tracts (Table 163.4).¹⁰⁵ Initial neurologic symptoms may include subtle changes in personality and cognition and paresthesias or pain near the exposure site. Rabies is rarely considered early in the differential diagnosis. In one series physicians considered rabies in only 3 of 21 patients on the first visit, despite an exposure history in many.¹⁰⁵ The prodrome typically lasts about 4 days, but up to 10 days may elapse before more specific symptoms and signs supervene.¹⁰⁵ Myoedema (mounding of part of the muscle struck with a reflex hammer, which then disappears in a few seconds) is present during the prodrome and persists throughout the disease.¹⁰⁶

Human rabies virus infections are divided into two forms: encephalitic (“furious”) and paralytic (“dumb”). The encephalitic form presents with the hydrophobia, delirium, and agitation that form the common picture of rabies. About a fifth of patients present with the paralytic form and have little clinical evidence of cerebral involvement until late in the course. The spinal cord and brainstem bear the brunt of the illness in the paralytic form. The pathogenetic distinction between the two types of rabies is unclear; it does not appear to be based on virologic or antigenic differences.¹⁰⁷ In either form the symptomatic course usually runs 2 to 14 days before coma supervenes. In one series of 32 patients the median duration of illness was 19 days.¹⁰⁸ On occasion, atypical features have been described that do not fit into these classic forms of rabies.¹⁰⁹ Atypical cases can present with sensory or motor deficits, choreiform movements of the bitten limb during the prodromal phase, focal brainstem signs, cranial nerve palsies, myoclonus, and seizures.^109,110

Not all infections may lead to death or even clinical illness as suggested by a study of Peruvians in the Amazon with a high incidence of bat bites¹¹¹; 6 of 63 residents without history of rabies vaccination were seropositive for rabies virus–neutralizing antibodies, suggesting prior subclinical infection.

Prodromes

En analyse multivariée, deux équipes n'ont retrouvé comme prodromes significatifs que les céphalées et les troubles visuels ^[40,41].

Enfin, il faut aussi rappeler la fréquence des crises inopinées : dans une série rétrospective incluant 53 femmes qui ont convulsé, une hypertension artérielle n'avait été notée que chez une seule des 21 femmes qui avaient consulté pendant la semaine précédant les convulsions ^[42]. Un travail récent collectant 214 E note l'absence totale de prodromes chez 21 % des femmes ^[32].

Prodromal Symptoms

Patients at risk for SCD can have prodromes such as chest pain, dyspnea, weakness or fatigue, palpitations, syncope, and a number of nonspecific complaints. Several epidemiologic and clinical studies have demonstrated that such symptoms can presage coronary events, particularly MI and SCD, and result in contact with the medical system weeks to months before SCD.

Attempts to identify early prodromal symptoms specific for SCD risk have not been successful. Although several studies have reported that 12% to 46% of fatalities occur in patients who had seen a physician 1 to 6 months before death, such visits are more likely to presage MI or nonsudden death, and most complaints responsible for these visits are not heart related. However, patients who have chest pain as a prodrome to SCD appear to have a higher probability of intraluminal coronary thrombosis at postmortem examination. Fatigue has been a particularly common symptom in the days or weeks before SCD in a number of studies, but this symptom is nonspecific. The symptoms that occur within the last hours or minutes before cardiac arrest are more specific for heart disease and may include symptoms of arrhythmias, ischemia, and heart failure.

Orbital Myositis

HD prodrome III: high/near

The prodrome subgroup, referred to as “high probability of diagnosis within 5 years” (> 85%) and “near motor diagnosis” (< 7 years), is the subgroup with the most pronounced rate of decline in all areas studied, known as HD prodrome III (prHD III) subgroup. This subgroup should be used for testing new treatments since change over time is significant and the measurement of every domain (motor, cognitive, magnetic resonance imaging (MRI) scan) is robust due to advanced disease. Burden scores in this subgroup are typically above 350. MRI volume changes are over 4% per year, and changes in cognitive and motor scores are great. Most cognitive measures show decline during this phase, with the most pronounced impact in time needed to complete tasks, smell identification, and time estimation, with noted decline also in decision making and visual perception.

Infection

Presentation

19 Describe the characteristic clinical picture of erythema nodosum

A prodrome of fever, chills, malaise, and arthralgia may precede the typical skin findings. Crops of red to blue tender nodules appear over the anterior shins. Lesions may be seen on the knees, ankles, thighs, and, occasionally, the lower extensor forearms and face. They may evolve through a spectrum of colors that resemble a bruise. Often the changes are misdiagnosed as cellulitis or are secondary to a traumatic event. This condition is associated with a variety of infectious (e.g., group A β-hemolytic streptococcus, tuberculosis) and noninfectious (e.g., ulcerative colitis, leukemia) causes.