Giddiness history

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Here is a comprehensive guide to taking a history of giddiness (dizziness/vertigo):

History Taking for Giddiness

1. Define the Symptom First

Never accept "dizziness" or "giddiness" as a final descriptor. Ask the patient to characterise it into one of three categories:
CategoryDescription
VertigoSensation of movement of self or surroundings (spinning)
Pre-syncope / LightheadednessFeeling faint, "about to pass out"
Disequilibrium / ImbalanceUnsteadiness without abnormal head sensation
Caution: patient descriptions can be unreliable and overlapping — timing and triggers are often more diagnostically useful than symptom type alone.
Bradley and Daroff's Neurology in Clinical Practice

2. Key History Questions

Onset & Timing

  • When did it first start?
  • Continuous or episodic?
  • Duration of each episode (seconds / minutes–hours / days)?
  • Frequency? Last episode?
  • Do symptoms fully resolve between episodes?

Triggers

  • Positional changes (rolling in bed → BPPV)?
  • Standing up (orthostatic hypotension)?
  • Head movements?
  • Sound or pressure changes (perilymph fistula)?
  • Salty food intake (Menière's disease)?
  • Stress, exercise, excitement (familial ataxia)?
  • Migraine triggers (light, stress)?

Mitigating / Exacerbating Factors

  • What makes it better or worse?
  • Does visual fixation suppress it?

Severity

  • Does it limit daily activities or cause falls?

3. Associated Symptoms

Ear (Labyrinthine) Symptoms

  • Hearing loss (unilateral or bilateral, fluctuating?)
  • Tinnitus (pulsatile or ringing?)
  • Aural fullness
  • Autophony
  • Otorrhoea / otalgia
  • Nausea, vomiting, sweating, diarrhea (autonomic features of true labyrinthine vertigo)

Neurological Symptoms (should NOT be present with pure labyrinthine vertigo — their presence points to a central cause)

  • Extremity weakness or numbness
  • Cranial nerve deficits (diplopia, facial weakness, dysphagia)
  • Headache / visual aura / photophobia / phonophobia
  • Memory loss or personality change
  • Ataxia

Cardiovascular

  • Palpitations (arrhythmia)
  • Chest pain
  • Syncope

4. Medication History

  • Current medications (aminoglycosides, loop diuretics, antihypertensives, antiepileptics — all ototoxic or vestibulotoxic)
  • Polypharmacy in the elderly is a major cause of chronic dizziness

5. Past Medical & Surgical History

  • Prior ear infections, ear surgery, head trauma
  • Hypertension, diabetes, cardiovascular disease
  • Autoimmune disease (relevant for immune-mediated labyrinthitis)
  • Migraines

6. Family History

  • Hereditary hearing loss or vestibular disorders
  • Familial ataxia syndromes

7. Social History

  • Noise exposure (occupational or recreational)
  • Tobacco and alcohol use
  • Caffeine/stimulant intake (can exacerbate tinnitus and dizziness)

8. Differential Diagnosis by Duration — Key Pointer

Vertigo differential by timing
Fig. 137.5 — Establishing a differential diagnosis with a chief complaint of vertigo (Cummings Otolaryngology)
DurationThink of
SecondsBPPV, vertebrobasilar insufficiency, vestibular migraine
Minutes–hoursMenière's disease, superior canal dehiscence, vestibular migraine
DaysLabyrinthitis, vestibular neuritis
Constant + focal neurologyStroke, MS, complicated migraine
Constant, no focal neurologyPolypharmacy, PPPD, cerebellar lesion, B12 deficiency, hypothyroidism, vision change

9. Summary Table for History Taking in Vertigo

DomainKey Questions
Symptom descriptionSpinning? Faintness? Imbalance?
Onset & durationSudden/gradual? Seconds/hours/days?
PatternContinuous or episodic? Frequency?
TriggersPositional? Standing? Sound?
Associated ear sxHearing loss, tinnitus, fullness, otorrhoea
Neurological sxWeakness, diplopia, headache, ataxia
Autonomic sxNausea, vomiting, sweating
MedicationsOtotoxics, antihypertensives, polypharmacy
PMH/FH/SHEar disease, migraine, cardiovascular, noise exposure
Cummings Otolaryngology Head and Neck Surgery; Bradley and Daroff's Neurology in Clinical Practice

Seizure history

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History Taking for Seizures

The clinical history is the cornerstone of seizure evaluation. Since the patient often has impaired consciousness during the event, obtaining a witness account is equally — sometimes more — important than the patient's own account.

1. Obtain History from Both Patient AND Witness

  • Interview patient and witness separately where possible to assess consistency
  • Witness's recollection may be distorted by panic — try to get more than one witness
  • Ask family if they have captured events on home video — invaluable
  • Construct the event in temporal order: Prodrome → Aura → Ictus (ictal phase) → Postictal
Bradley and Daroff's Neurology in Clinical Practice

2. The Event Itself — Phase by Phase

Prodrome (hours to days before)

  • Mood change, irritability, headache, sleep disturbance?
  • Not part of the seizure itself but may warn of an impending event

Aura (seconds before — focal onset marker)

  • Any warning the patient noticed just before losing awareness?
  • Type of aura localises the epileptogenic zone:
Aura TypeLikely Localisation
Epigastric rising sensationTemporal lobe (mesial)
Déjà vu / jamais vuTemporal lobe
Fear / psychic symptomsTemporal (amygdala)
Visual (lights, colours)Occipital lobe
Tingling / numbnessParietal lobe
Motor twitching of one limbFrontal/motor cortex
Olfactory hallucinationTemporal (uncus)

Ictal Phase (the seizure itself — from witness)

  • How did it begin? (focal jerking, eye deviation, head turn, automatisms?)
  • Consciousness — fully aware, partially aware, or lost?
  • Motor features: tonic (stiffening), clonic (rhythmic jerking), tonic-clonic, atonic (drop)?
  • Automatisms: lip smacking, chewing, fumbling, picking, wandering?
  • Eye deviation or head turn (lateralising — often contralateral to focus)
  • Vocalisations or cry at onset (tonic-clonic)?
  • Tongue biting (lateral biting = tonic-clonic seizure; tip biting = non-epileptic)
  • Urinary or fecal incontinence?
  • Colour: cyanosed, flushed, pale?
  • Duration of the event?

Postictal Phase

  • Confusion, drowsiness, amnesia?
  • Duration of postictal confusion (longer = more severe seizure)
  • Headache?
  • Muscle soreness / aching?
  • Todd's paralysis (focal weakness after focal motor seizure)?
  • Able to recall the event? (Absent in GTC; present in focal aware seizures)
Absence seizures are a notable exception — no postictal phase

3. Seizure Frequency and Pattern

  • First-ever seizure or recurrent?
  • Age at first seizure
  • Total number of seizures / frequency
  • Clustering? (multiple in 24 hours)
  • Any change in seizure type or frequency recently?
  • Longest seizure-free interval?
  • Status epilepticus ever?

4. Precipitating Factors / Triggers

TriggerRelevance
Sleep deprivationVery common — lowers seizure threshold
Alcohol (use or withdrawal)Direct proconvulsant effect
Drug use / withdrawalBenzodiazepine, antiseizure drug non-compliance
Fever / infectionEspecially in children
Flashing lights / TV screensPhotosensitive epilepsy
Menstrual cycleCatamenial epilepsy
Stress / emotional upsetCommon trigger
Missed medicationMost common cause of breakthrough seizures
HyperventilationTriggers absence seizures
Exercise, sudden movementParoxysmal dyskinesia vs. seizure

5. Past Medical History

  • Perinatal/birth history: hypoxia, prematurity, neonatal seizures
  • Developmental milestones: regression or delays suggest underlying syndrome
  • Febrile seizures in childhood (associated with mesial temporal lobe epilepsy)
  • CNS infections: meningitis, encephalitis, brain abscess
  • Head trauma: loss of consciousness, depressed skull fracture, intracranial pathology
  • Stroke or cerebrovascular disease (especially in elderly-onset epilepsy)
  • Brain tumours or neurosurgery
  • Neurocutaneous disorders: tuberous sclerosis, neurofibromatosis, Sturge-Weber
  • Metabolic disorders: hypoglycaemia, hyponatraemia, renal/hepatic failure
  • Psychiatric history: anxiety, depression (non-epileptic attack disorder common)

6. Drug and Medication History

  • Current antiseizure medications (ASMs) and compliance
  • Recent dose changes or new prescriptions
  • Drugs that lower seizure threshold: tramadol, bupropion, clozapine, ciprofloxacin, theophylline, isoniazid
  • Drug-drug interactions with ASMs
  • Recreational drugs, alcohol (especially withdrawal)
  • Women of reproductive age: pregnancy (affects ASM clearance), oral contraceptive interaction with enzyme-inducing ASMs

7. Family History

  • Afebrile seizures in first- or second-degree relatives
  • Febrile seizures
  • Other paroxysmal disorders (migraine, syncope)
  • Ask a senior female relative for best family history recall
  • Genetic epilepsy syndromes (Dravet, GEFS+, juvenile myoclonic epilepsy)

8. Social History

  • Driving (legal obligation to report seizures in most jurisdictions)
  • Occupation (working at heights, with machinery, near water — safety risk)
  • Alcohol and substance use
  • Sleep habits
  • Psychosocial stressors

9. Seizure Classification (ILAE 2017) — guides history taking

OnsetType
Focal onsetAware (previously: simple partial) or Impaired awareness (previously: complex partial) → may evolve to bilateral tonic-clonic
Generalised onsetAbsence, myoclonic, tonic, clonic, tonic-clonic, atonic
Unknown onsetTonic-clonic, behaviour arrest, others

10. Differential Diagnosis — Key Distinguishing Questions

ConditionClues from History
SyncopeProdrome of nausea/pallor/sweatiness; triggered by pain/standing; brief confusion; quick recovery
Non-epileptic attack disorder (NEAD/pseudoseizure)Psychiatric history, prolonged events, suggestible triggers, eyes closed during event, no postictal confusion, high symptom burden
TIANegative symptoms (weakness, numbness), no postictal phase
Migraine with auraVisual aura evolves slowly; headache follows
Narcolepsy/cataplexyTriggered by emotion; preserved consciousness throughout
BPPV/panic attackPositional or anxiety context; no loss of consciousness

Summary Checklist

DomainKey Points
SourcePatient + witness + video
PhasesProdrome → Aura → Ictus → Postictal
Ictal featuresOnset, motor type, awareness, lateralising signs, autonomic, duration
PostictalConfusion duration, Todd's paresis, tongue bite, incontinence
PatternFrequency, clustering, change over time
TriggersSleep, alcohol, drugs, fever, menses, missed medication
PMHBirth, febrile seizures, CNS infection, head injury, stroke
MedicationsCurrent ASMs, compliance, interactions, pregnancy
Family HxSeizures, febrile convulsions, paroxysmal disorders
SocialDriving, occupation, safety, alcohol/drugs
Bradley and Daroff's Neurology in Clinical Practice; Rosen's Emergency Medicine
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