management principles of neurological emergencies

2. Neurological Emergencies
DR MUBASHAR SULTAN HASHMI
SPECIALIST ICU/KKFHJ

3. Neurological Emergencies
 Acute Ischemic Stroke
 Intracranial Hemorrhage
 Status Epilepticus
 Guillan-Barre Syndrome
 Acute Myelopathy
 Myasthenic Crisis

4. Acute Ischemic Stroke
 AIS is caused by the sudden loss of blood circulation to an
area of the brain resulting in ischemia and corresponding
loss of neurological function.
 Within seconds to minutes of loss of perfusion, an
ischemic cascade is unleashed resulting in a central area
of irreversible infarction surrounded by an area of
potentially reversible ischemic penumbra.
 Goal of treatment : To preserve the area of oligemia in the
ischemic penumbra. This is done by limiting the severity
of injury (neuronal protection) and by restoring blood flow
to the penumbra.

5. Presentation
 No clinical feature reliably distinguishes AIS from
hemorrhagic stroke, though headache, N/V, and
altered mental status make hemorrhagic stroke more
likely.
 Common symptoms of AIS include the abrupt onset
of hemiparesis, monocular visual loss, ataxia, vertigo,
aphasia, or sudden depressed level of
consciousness.
 Establishing the onset of symptoms is essential when
considering possible thrombolytic therapy.

6. Transient Ischemic Attack
 TIA’s are defined as a transient ischemic neurological
deficit that resolves within 24 hours
 80% resolve within 60 minutes
 TIA’s precede 30% of AIS
 Left untreated, 30% of TIA’s progress to AIS (20%
within the first month and 50% within the first year)

7. Physical Exam.
 Goal of PE is to look for extra cranial causes of AIS and
to distinguish AIS from stroke mimics (seizures, tumors,
toxic-metabolic disturbances, positional vertigo, etc).
 HEENT: Look for trauma signs and nuchal rigidity, listen
for cranial or cervical bruits, evaluate pulse strength.
Fundoscopy to look for emboli, hemorrhage,
papilledema.
 C/V: Signs of CHF, Atrial fibrillation, arrhythmias.
 Ext: Signs of venous thrombosis and arterial emboli.

8. Assessing Consciousness
AVPU
GLASGOW COMA SCALE

9. Rapid Assessment
A Alert
V responds to Voice
P responds to Pain
U Unresponsive

10. Neurological chart
 GCS top section
 Temperature/BP/pulse/respiratory rate
 Pupil size / reaction to light
 Limb movement – arms and legs

11. Glasgow Coma Scale
 Assesses patient’s neurological condition
 Value range 3 to 15
 3 totally comatose patient
 15 fully alert patient

12. Classification of Brain Injury
According to Glasgow Coma Scale
(GCS) (HICKEY 2003)
MILD
GCS 13-15
MODERATE
GCS 9-12
SEVERE
GCS 3-8

13. Eye opening
 Spontaneous = 4
 To speech = 3
 To pain = 2
 None = 1

14. Verbal response
 Orientated = 5
 Disorientated = 4
 Monosyllabic = 3
 Incomprehensive = 2
 None = 1

15. Motor response
 Obeys commands = 6
 Localises pain = 5
 Withdrawal to pain = 4
 Flexion to pain = 3
 Extension to pain = 2
 None = 1

16. Posturing

17. Neurologic exam: AIS
 Goal is to establish baseline for monitoring response to
therapy and to determine size and location of AIS
 MS, CN, Motor, Coordination, Sensory and Gait need to be
covered, however speed is of the essence!
 MCA: Contralateral : Hemiparesis, Hemianopsia and
Sensory loss
Ipsilateral: Gaze preference.
Dominant Hemisphere: Aphasia
Non-Dominant Hemisphere: Hemi-neglect and
cortical sensory deficits

18. Neurologic exam: AIS
 ACA: Disinhibition, primitive reflexes, contralateral
hemiparesis (legs>arms), urinary incontinence.
 PCA: Contralateral hemianopsia, cortical blindness,
altered mental status, impaired memory.
 Vertebrobasilar: Vertigo, nystagmus, ataxia.
Crossed findings (ipsilateral cranial nerve deficits
along with contralateral long track signs).
 Lacunar Infarcts: Pure motor, pure sensory,
ataxia/hemiparesis.

19. Work up: AIS
 Labs: CBC with platelets, CMP, PT, PTT, cardiac
biomarkers, EKG.
 Imaging: Emergent non-contrast CT
 Distinguishes hemorrhagic from ischemic stroke
 Defines age and anatomic distribution of stroke
 Large hypodense area seen within 3 hours brings into
question of timing of AIS and may predict poor outcome
 Hyperdense MCA sign

20. Differential diagnosis for altered conscious
level
I: Infection - Sepsis, encephalitis, meningitis, syphilis, central nervous system (CNS) abscess,
malaria
W: Withdrawal - Alcohol, barbiturates, sedative-hypnotics
A: Acute Metabolic and endocrine - Acidosis, electrolyte disturbance, hepatic or renal failure,
magnesium, calcium: diabetes, adrenal, thyroid
T: Trauma – head trauma, burns, abuse
C: CNS– Hemorrhage stroke, seizures, tumor
H: Hypoxia/Hypercarbia – COPD, Pneumonia CO
D: Deficiencies- Vitamin B12, thiamine
E: Environmental: Hypothermia, hyperthermia;
A: Acute Vascular - Hypertensive emergency, subarachnoid hemorrhage, sagittal vein
thrombosis
T: Toxins/Drugs - Medications, street drugs, alcohol, pesticides

21. Hyperdense MCA Sign

23. Large Cortical Hypodensity

24. Other imaging studies: AIS
 CT Angiography
 MRI:
 Diffusion-Perfusion mismatch (correlates to the core area of
infarction and surrounding area of the ischemic penumbra)
 More sensitive than CT to early ischemic changes
 MR Angiography
 Conventional Cerebral Angiography
 Echocardiography: (CHF, akinetic wall, vegetation/clots,
septal defects, PFO)
 Carotid Doppler Ultrasound: Carotid stenosis evaluation

25. Treatment
 ABCD’s
 Airway: Intubation for GCS < 8 or lack of airway
protective reflexes
 Breathing: O2 if hypoxic. Keep PCO2 32-36 mmHg
 Circulation: Maintain adequate CPP (MAP-ICP).
 Do not treat HTN unless > 200/120
 D = Dextrose. Maintain normoglycemia (even if insulin is
needed) as hyperglycemia worsens neurological
outcome

26. Coma cocktail - DONT
 Dextrose
 Oxygen
 Naloxone
 Thiamine
 Flumazanil?

27. Treatment : AIS
 Fever: Hyperthermia worsens ischemic injury
 Cerebral edema: Peaks 72-96 hours. Hyperventilation
can decrease CPP.
 Mannitol may leak across compromised BBB. No
evidence of benefit for steroids.
 Decompressive craniectomy and resection of necrotic
tissue may be indicated, especially in the setting of
hemorrhagic transformation.
 Seizure control: Prophylactic AED is not indicated unless
malignant elevated ICP is present

28. Acute Thrombolysis:AIS
 Balance restoration of blood flow and hemorrhage risk
 No evidence of hemorrhage on CT
 Hypodensity on CT < 1/3 of hemisphere
 Onset of symptoms within 3 hours of rTPA use
 SBP < 185 DBP < 110
 INR < 1.7, Platelets > 100,000, No ASA or
anticoagulation, No trauma or recent surgery
 rTPA: 0.9 mg/kg IV over 60 minutes with 10% of
dose given over the 1st minute

29. Strategies for Reducing Future Strokes
 Anti-Platelet Therapy
 Warfarin: (Atrial Fibrillation, Arterial Dissection)
 Carotid Endarterctomy / Stent Placement
 PFO Closure
 Reducing Stroke Risk Factors
(Hypercholesterolemia, Hypertension, Diabetes,
Obesity, Lack of Exercise, Smoking, OCP’s)

30. Intracranial Hemorrhage
Location of Hemorrhage
 Intraventricular Hemorrhage
 Intraparenchymal Hemorrhage
 Subarachnoid Hemorrhage
 Subdural Hematoma
 Epidural Hematoma

31. Intraventricular Hemorrhage
 Accounts for 3% of all non-traumatic ICH
 Hypertension is the most common etiology
 Often results from an intraparenchymal hemorrhage
that extends into the ventricular system
 S/S: Headache, N/V, Progressive deterioration of
consciousness, raised ICP, Nuchal rigidity
 Survivors may develop post-hemorrhagic
hydrocephalus

32. Intraparenchymal Hemorrhage
 Basal Ganglia Hemorrhage
 Contralateral hemiparesis, hemichorea, hemisensory loss, and
hemi-neglect are common neurological deficits

33. Intraparenchymal Hemorrhage
 Thalamic Hemorrhage
 Contralateral hemiparesis, hemisensory loss and
depressed LOC (wake center) are common
deficits

34. Intraparenchymal Hemorrhage
Pontine Hemorrhage
 Abrupt onset of coma, pinpoint pupils, autonomic
instability, horizontal gaze paralysis, and
quadriparesis
 The miotic pupils and depressed LOC may mimic
opiate overdose

35. Pontine Intraparenchymal Hemorrhage

36. Intracranial Hemorrhage
 Cerebellar Hemorrhage
 Sudden onset of vertigo, severe N/V, and ataxia
 altered mental status and coma over a few hours
 Obstructive hydrocephalus can contribute to brainstem
herniation
 Urgent posterior fossa decompression is essential for survival

37. Intraparenchymal Cerebellar Hemorrhage

38. Lobar Intraparenchymal Hemorrhage

39. Etiology: Intraparenchymal Hemorrhage
 Hypertension is the #1 cause in adults
 Anticoagulation and Anti-Platelet Meds
 Systemic anticoagulated states (eg. DIC)
 Aneurysms, AVM’s, Cavernous Angiomas

40. Treatment: ICH
 ABCD’s
 Intubation??
 Treat Hypertension to keep SBP < 160 mmHg
 Fluid and Electrolyte Management
 Use Normal Saline, avoid Dextrose
 Watch for SIADH and Cerebral Salt Wasting
 Prevent Hyperthermia
 Seizure Prophylaxis
 Correct Underlying Coagulopathy
 FFP, platelet Infusions, Vitamin K

41. Treatment :ICH
 Recombinant Factor VII
 Dosing ranges between 40 and 160 micrograms
 Beneficial if given within 4 hours of onset
 Risk of myocardial infarction and AIS
 Management of ICP
 Hyperventilate to keep PaCO2 around 30 mmHg
 Avoid Mannitol (can leak into hematoma)
 External Ventricular Drain (if hydrocep0halus present)
 Surgical Evacuation of Hematoma (controversial)

42. Subarachnoid Hemorrhage
 Aneurysmal rupture accounts for 80% of cases
 Risk Factors
 Advancing age, Smoking, HTN, Cocaine use, Hypertension,
Heavy Alcohol use, Connective Tissue Disorders, Sickle Cell
Disease, First Degree Relatives with Aneurysms
 Fatality rate is 50% within 2 weeks
 30% of survivors require lifelong care
 15% of patients will have > 1 aneurysm
 Outcome largely dependent on clinical presentation
and CT findings

43. Subarachnoid Hemorrhage
• Sudden-Onset “Thunderclap
Headache”
• “Worst Headache of my life”
• CN III palsy (p. comm aneurysm)
• CN VI palsy (raised ICP)
• Retinal Hemorrhages
• Altered Mental Status
• Nuchal Rigidity
Clinical
presenting
signs

44. Diagnostic Work Up
 CT Imaging
 Will pick up > 90% SAH (get thin cuts through skull
base)
 Sensitivity drops to < 50% after 2 weeks
 Carefully evaluate basilar cisterns for hemorrhage

46. Diagnostic Work Up
 Lumbar Puncture
 Perform if high index of suspicion and negative CT
 Elevated Opening Pressure
 Increased RBC count that does not “clear” between tubes one and tube four
 Xanthochromia (rule of 2’s)
 Starts at 2 hours, Peaks at 2 days, Clears by 2 weeks

47. Diagnostic Work Up
 Angiography
 Digital Subtraction Angiography is gold standard
 CT Angiography
 MR Angiography
 Look for Multiple Aneurysms

48. CT Angiogram

49. MR
Angiogram

50. Treatment
 General Measures
 ABCD’s
 Intubation for GCS < 9
 Treat HTN: SBP 90-140 prior to aneurysm treatment, < 200 mmHg after Rx
 Glucose between 80 and 120 mg/dl
 Euvolemia (CVP 5-8 mmHg unless vasospasm, then CVP 8-12 mmHg)
 Temperature
 Quiet Room / Sedation
 GI (H2 blocker, stool softener, NPO)
 Vasospasm
 Nimodipine 60 mg po q 4 hrs for 21 days
 Seizures (Phenobarbital or Lorazepam)

51. Treating the Aneurysm
 Surgical Intervention
 Endovascular Coiling

52. Status Epilepticus
Definitions
 A single seizure or back-to-back seizures
without return of consciousness lasting
> 45 minutes (primate studies)
>30 minutes (WHO definition)
>10 minutes (working definition)

53. Etiologies
 Idiopathic (24%) No precipitating event, pt is
neurologically and developmentally normal
 Febrile (24%) Includes “febrile seizures” and
seizures in the setting of a febrile illness
 Prior neurological insult or developmental
brain malformation

54. Etiologies
 Vascular
 Stroke (Hemorrhagic > Ischemic)
 Subarachnoid Hemorrhage
 Hypoxic Ischemic Encephalopathy
 Toxic
 Cocaine and other sympathomimetics
 Alcohol withdrawal
 Various Medications (Isoniazid, TCA’s, various
chemotherapy agents)
 AED non-compliance or withdrawal

55.  Metabolic
 Hyper or Hypo-Natremia
 Hypoglycemia
 Hypocalcemia
 Liver or Renal failure
 Infectious
 Meningoencephalitis
 Brain Abscess
 Trauma
 Neoplastic

56. Status Epilepticus
 History
 Fever, pre-existing epilepsy, trauma, baseline AED’s and their dosing
 Physical Exam
 Signs of trauma, nuchal rigidity, end organ injury
 Subtle signs of seizures (tachycardia, pupil dilation and hippus, nystagmus,
irregular respirations)
 Work Up
 Lytes, glucose, AED levels, CPK, LFT’s, ABG, ammonia
 CT of brain
 LP (when stable) if indicated. Empiric antibiotics.

57. Treatment
ABCD’s
Airway: Risk of aspiration,
suction to bedside
Breathing: Give
supplemental O2
C/V: Initial tachycardia
giving way to hypotension
(especially when
Benzos or Barbiturates
are given)
Dextrose: Symptomatic
hypoglycemia is causing
irreversible brain
injury until corrected

58. Anticonvulsant therapy
 Benzodiazepine Therapy (10 minutes)
 Long-Acting AED Therapy (10 to 30 minutes)
 Refractory Status Therapy (>30 minutes)

59. Benzodiazepine Therapy
 Lorazepam
 0.1 mg/kg max: 4 mg/dose
 Has 8 hour effective t½
 Diazepam
 0.3 to 0.5 mg/kg max: 10 mg/dose

60. Long-Acting Anticonvulsant Therapy
 Phenytoin
 20 mg/kg over 20 minutes (regardless of weight)
 C/R monitor during load
 No dextrose in line
 Extravasation injuries are severe

61. Long-Acting Anticonvulsant Therapy
 Phenobarbital
 20 mg/kg over 20 minutes
 Watch for respiratory suppression (especially if the patient has received
Benzodiazepines)
 Watch for hypotension
 Good for Febrile Status Epilepticus

62. Refractory Status
 Secure airway
 Transfer to ICU
 Extra lines for hypotension treatment
 EEG Monitoring (electrical-clinical dissociation)
 Medications
 Pentobarbital
 Other agents (Midazolam drip, Propofol, Lidocaine,
inhalation anesthetics, other AED’s)

63. Guillan-Barre´Syndrome
 Progressive ascending weakness along with
various cranial neuropathies
 Areflexia
 Minimal sensory deficits (though radicular pain is
common)
 Progression over days to 4 weeks
 Preceding infection or Immunization: 1 to 4
weeks prior to onset of weakness (C. jejuni,
CMV, Mycoplasma, dT, OPV, VZV)

64. Physical Exam
 Bulbar and Respiratory Compromise
 Relatively Symmetric Ascending Weakness
 Diminished/Absent DTR’s
 No Sensory Level
 Radicular Pain/Paresthesias
 Autonomic Dysfunction: Increased or Decreased SNS or
PNS Function (tachy-brady arrhythmias,
hyper/hypotension, urinary retention,
decreased GI mobility)

65. Laboratory workup
 CSF: Albuminocytological Dissociation
 Elevated Protein without Pleocytosis
 Nerve Conduction:

66. Treatment
ABC’s
 Airway/Breathing: (Serial Examinations)
 Forced Vital Capacity: (want > 15 ml/kg)
 Negative Inspiratory Force (want > - 40 mmHg)
 ABG’s : Look for rising Pa CO2
 Clinical Exam (accessory muscles, SOB, diminished exhalation strength)
 Elective Intubation if Respiratory Insufficiency or significant Bulbar Weakness

67.  ABC’s
 Cardiovascular
 BP Monitoring
 Careful when treating hypo or hypertension
 Excessive Vagal Response with GI pain, Intubation, Tracheal
Suctioning and other Procedures
 ICU Monitoring Until Patient Reaches Nadir of Weakness

68.  IVIG
 5 day infusion of 0.4 g/kg per day
 Plasmapharesis
 5 exchanges (40-50 ml/kg) given on alternate days using saline and
albumin as replacement fluid
 No Role for Steroids

69. Outcome-GBS
 10% to 20% require mechanical ventilation
 Mortality 2% to 5%
 After nadir, plateau phase lasts 2-4 weeks
 70% complete recovery within 1 yr, 82% by 2 yrs
 3% will go on to have relapse (CIDP)

70. Transient loss of consciousness-
syncope

71. Definition
Syncope is a symptom, the defining clinical
characteristics of which are:
• transient
• self-limited loss of consciousness
• leads to falling
• onset is relatively rapid
• recovery is spontaneous, complete, and
usually prompt
The underlying mechanism is a transient global
cerebral hypoperfusion

72. Classification of Syncope
 Syncope must be differentiated from other
“non-syncopal” conditions which also lead
to transient loss of consciousness.
 Pathophysiological classification is based on
the principal causes of the transient loss of
consciousness.

73. Real or apparent transient loss of consciousness
Syncope Non-syncopal attacks
• With partial or complete
loss of consciousness
• Without any impairment of
consciousness

74. Loss of consciousness: Syncope{C AUSES}
Neurally-mediated Vasovagal faint (common faint):
- classical
- non-classical
Carotid sinus syncope
Situational Faint
Glossopharyngeal neuralgia
Orthostatic hypotension Autonomic failure (primary, secondary,
drug and alcohol, post-exercise, post-
prandium, volume depletion)
Cardiac arrhythmias Bradycardia (sinus & AV diseases)
Tachycardia (atrial & ventricular)
Inherited (long QT, Brugada s.)
Implanted device malfunction
Drug-induced pro-arrhythmias
Structural cardiac Valvular disease, Acute ischaemia,
Obstructive diseases, Tamponade,
Pulmonary embolism, Aortic dissection
Cerebro-vascular Vascular steal syndromes

75. Loss of consciousness: II - Non-syncopal
Partial or complete loss of consciousness
Metabolic Hypoxia,hyperventilation,
hypoglycemia
Epilepsy
Intoxication
Vertebro-basilar TIA
Any impairment of consciousness
Falls
Cataplexy
Drop attacks
Psychogenic ‘pseudo-syncope’ Fictitious disorders, malingering
and conversion
Carotid TIA

76. Diagnosis

77. Management strategy
• Initial evaluation
(history, physical exam, ECG & BP supine/upright)
• Laboratory investigations guided by the
initial evaluation
• Treatment
The diagnostic strategy based on the initial
evaluation

78. Initial evaluation
(History, physical exam, ECG & BP supine/upright)
Diagnosis

79. Initial evaluation
Question 1
• Syncope or non-syncopal attack ?
Question 2
• Is heart disease present or absent ?
Question 3
• Which history of syncope ?
3 key questions:

80. Initial evaluation
Important historical features
1 - Questions about circumstances just prior to attack
• Position (supine, sitting or standing)
• Activity (supine, during or after exercise)
• Situation (urination, defecation, cough or swallowing)
• Predisposing factors (e.g., crowded or warm places, prolonged
standing, post-prandial period)
• Precipitating events (e.g., fear, intense pain, neck movements)
2 - Questions about onset of attack
• Nausea, vomiting, feeling of cold, sweating, aura, pain in neck
or shoulders
3 - Questions about attack (eyewitness)
• Skin colour (pallor, cyanotic)
• Duration of loss of consciousness
• Movements (tonic-clonic, etc)
• Tongue biting

81. Initial evaluation
Important historical features
5 - Questions about end of attack
Nausea, vomiting, diaphoresis, feeling of cold, confusion,
muscle aches, skin colour, wounds
6 - Questions about background
• Number and duration of syncopes
• Family history of arrhythmogenic disease
• Presence of cardiac disease
• Neurological history (Parkinsonism, epilepsy, narcolepsy)
• Internal history (diabetes, etc.)
• Medication (hypotensive and antidepressant agents)

82. Initial evaluation
Diagnostic criteria
• Vasovagal syncope is diagnosed if precipitating
events such as fear, severe pain, emotional
distress, instrumentation and prolonged standing
are associated with typical prodromal symptoms.
• Situational syncope is diagnosed if syncope
occurs during or immediately after urination,
defaecation, cough or swallowing.
• Orthostatic syncope is diagnosed when there is
documentation of orthostatic hypotension
associated with syncope or presyncope.

83. Initial evaluation
ECG diagnostic criteria
Syncope due to cardiac arrhythmia is diagnosed
in case of:
• Symptomatic sinus bradycardia <40 beats/min
or repetitive sino-atrial blocks or
sinus pauses >3 s.
• Mobitz II 2nd or 3rd degree atrioventricular block.
• Alternating left and right bundle branch block.
• Rapid paroxysmal supraventricular tachycardia
or ventricular tachycardia.
• Pacemaker malfunction with cardiac pauses.

84. Initial evaluation
ECG diagnostic criteria
Syncope due to cardiac ischemia
is diagnosed when symptoms are present with
ECG evidence of acute myocardial ischaemia
with or without myocardial infarction,
independently of its mechanism (*).

85. Clinical and ECG features that suggest a cardiac syncope
 Presence of severe structural heart disease
 Syncope during exertion or supine
 Palpitations at the time of syncope
 Suspected VT (e.g. heart failure or NSVT)
 BBB
 Mobitz 1 second degree AVB
 Sinus bradycardia <50 bpm
 WPW
 Long QT
 ARVD or Brugada Syndrome

86. Clinical and ECG features that suggest a neurally-mediated
syncope
 Absence of cardiac disease.
 Long history of syncope.
 After sudden unexpected unpleasant sight, sound,
or smell.
 Prolonged standing or crowded, warm places.
 Nausea, vomiting associated with syncope.
 During or in the absorptive state after a meal.
 After exertion.
 With head rotation, pressure on carotid sinus.

87. Laboratory Investigations
Diagnosis

88. Certain or suspected heart disease
yes no
Cardiac evaluation
-Echocardiogram
-ECG monitoring
-Exercise test
-EP study
-ILR
NM evaluation
-Carotid sinus massage
-Tilt testing
-ATP test
-ILR

89. Treatment

90. Treatment of Syncope:
General Principles
 Principal goals of treatment:
 Prevent recurrences
 Reduce risk of mortality
 Additional goals:
 Prevent injuries associated with recurrences
 Improve quality of life

91. Neurally-mediated syndromes: therapy
Initial treatment:
Education and reassurance
Sufficient for most
No treatment Single syncope and no high
risk settings
Additional treatment High risk or high frequency
settings
Recommendations

92. Treatment of Orthostatic
Hypotension
CAUSE TREATMENT
Drug-induced
autonomic
failure
Eliminate the offending
agent
Primary &
secondary
autonomic
failure
Modify physical factors
that influence systemic
blood pressure*

93. Treatment of Cardiac Arrhythmias
as Primary Cause
 Treatment Goals:
 Prevention of symptom recurrence
 Improvement of quality of life
 Reduction of mortality risk

94. Treatment of Cardiac Arrhythmias
Cardiac pacemaker therapy is indicated
 Elimination of drugs that may increase susceptibility to
bradycardia should be considered
Catheter ablation for control of atrial arrhythmias
Sinus node dysfunction
(including bradycardia/tachycardia syndrome)

95. Metabolic Disturbances:
Hyperventilation
Hyperventilation resulting in hypocapnia and
transient alkalosis may be responsible for
confusional states or behavioral disturbances.
Clearcut distinction between such symptoms and
syncope may be difficult .
Frequently associated with anxiety episodes
and/or ‘panic’ attacks.
Recurrent faints associated with hyperventilation
should justify a psychiatric consultation.