Rosen & Barkin's 5-Minute Emergency Medicine Consult (726 page)

There is no known effective therapy for TGA

• TGA is a self-limited, relatively benign entity
  
• Observe the patient for improvement
  
• Assuming a true diagnosis of TGA, no acute treatment beyond reassurance of patient and family is indicated
  

Not applicable

Not applicable

FOLLOW-UP

• Admission for further observation for patients without significant improvement at the time of disposition
  
• Patients with uncertain diagnosis
  
• Patients showing a trend toward resolution but who have suboptimal social support at home
  

• A clear diagnosis of TGA
  
• Resolving or resolved amnesia
  
• Good social support
  

• Recurrence rate of TGA is 8%
  
• Refer patients with recurrent episodes of TGA to a neurologist:
  
  • May benefit from ambulatory EEG to workup epilepsy
    

Given median age of TGA patients (60 yr), follow-up with primary care provider for general cardiovascular risk factor modification may be beneficial:

• No follow-up specific to TGA is indicated
  
• See “Issues for Referral” for patient with recurrent episode of TGA
  

• TGA is a distinct and relatively benign entity:
  
  • Acute onset of isolated anterograde amnesia
    
  • Resolves spontaneously
    
• Be aware of subtle features that may suggest a more pathologic alternative diagnosis:
  
  • Short, recurrent episodes or automatisms in epilepsy
    
  • Cognitive impairment with encephalopathy
    
  • Subtle neurologic signs in encephalitis or TIA
    
• If there is uncertainty regarding the diagnosis, the highest yield tests are multimodal MRI and EEG
  

• Bartsch T, Deuschl G. Transient global amnesia: Functional anatomy and clinical implications.
  Lancet Neurol.
  2010;9:205–214.
  
• Hunter G. Transient global amnesia.
  Neurol Clin.
  2011;29:1045–1054.
  
• Kirshner HS. Transient global amnesia: A brief review and update.
  Curr Neurol Neurosci Rep.
  2011;11:578–582.
  
• Markowitsch HJ, Staniloiu A. Amnesic disorders.
  Lancet.
  2012;380:1429–1440.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Delirium
  
• Dementia
  

CODES

• 437.7 Transient global amnesia
  
• 780.93 Memory loss
  

BASICS

• TIA – an episode of reversible neurologic deficit caused by a temporary decrease in blood flow to an area of the central nervous system (CNS)
  
• Classically described as symptoms lasting <24 hr, but most TIA symptoms resolve in <1 hr
  
• A warning for stroke, as 12–30% of strokes will be preceded by TIA
  

• Transient decrease in perfusion to an area of the CNS, which can be caused by:
  
  • Thrombosis in medium to large arteries with atherosclerosis (25%)
    
  • Intracranial small vessel disease (25%)
    
  • Embolic cause from the heart (20%)
    
  • Miscellaneous, including arterial dissection, vasculitis, and hypercoagulable states (5%)
    
  • No clear predisposing vascular cause found (25%)
    

DIAGNOSIS

• Symptoms are determined by the vascular territories which are affected
  
• Large vessel TIA syndromes:
  
  • Anterior cerebral artery (ACA) – unilateral motor/sensory loss to leg > arm, disinhibition
    
  • Middle cerebral artery (MCA) – unilateral motor/sensory loss to face/arm > leg, aphasia if dominant hemisphere, neglect if nondominant hemisphere, homonymous hemianopsia
    
  • Posterior cerebral artery (PCA) – homonymous hemianopsia, may have alexia, prosopagnosia (can’t recognize faces)
    
  • Anterior inferior cerebellar artery (AICA) – unilateral deafness, vertigo, tinnitus, vomiting, ipsilateral facial weakness and limb ataxia, contralateral decrease in pain and temperature sensation
    
  • Posterior inferior cerebellar artery (PICA) – unilateral palatal weakness, unilateral limb ataxia, unilateral Horner's syndrome, decreased pain/temperature sensation on contralateral body:
    
    • Wallenberg syndrome
      
  • Vertebrobasilar artery – ataxia, oculomotor palsies, facial paresis, loss of consciousness, quadriplegia
    
  • Carotid artery – unilateral motor/sensory loss to face/leg/arm, aphasia if dominant hemisphere, neglect if nondominant hemisphere, homonymous hemianopsia
    
• Small vessel TIA syndromes:
  
  • Amaurosis fugax – transient monocular blindness from occlusion of ophthalmic branch of internal carotid
    
  • Lacunar infarcts – occlusion of a deep penetrating artery of the brain. Usually produce pure motor or pure sensory deficits
    
    • Internal capsule – hemiparesis or dysarthria with clumsy hand
      
    • Corona radiata – hemiparesis
      
    • Pons – dysarthria with clumsy hand
      
    • Thalamus – sensory loss to 1 side of the body
      

• Historical features suggestive of TIA:
  
  • Sudden onset
    
  • Short duration (as >60% of events last <1 hr)
    
  • Negative symptoms – CNS is underperfused and therefore, not functioning, so TIA syndromes generally produce loss of neurologic function – i.e., weakness or aphasia
    
  • Symptoms are focal, related to specific vascular territory
    
• Historical features not suggestive of TIA:
  
  • Gradual onset
    
  • Positive symptoms – increased neurologic function in a particular area, such as convulsion, tingling, or twitching, suggests increased CNS activity as with migraine or seizure
    

• Detailed neurologic exam: Strength, sensation, coordination, gait, naming/speech, and visual fields
  
• Persistent neurologic deficits suggest acute stroke rather than TIA
  
• The National Institute of Health Stroke Scale (NIHSS) is a reliable and easily repeatable neurologic exam (
  http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf
  )
  

• Rapid history and physical exam including detailed neurologic exam
  
• Fingerstick glucose – hypoglycemia can produce focal neurologic deficits
  
• Noncontrast CT head – rule out hemorrhage
  
• If patients present with persistent deficits, obtain STAT neurologic consultation with concern for acute stroke rather than TIA
  

• Glucose
  
• Chemistry panel – check Na, renal function
  
• CBC – exclude anemia, polycytosis
  
• Troponin – rule out concomitant ACS or demand ischemia
  
• Hemoglobin A1C and fasting lipid panel for patients being admitted/observed
  

• CT:
  
  • Upon arrival to ED, STAT noncontrast head CT to rule out CNS hemorrhage
    
• MRI:
  
  • Up to 50% of patients that clinically have a TIA will have evidence of infarction on MRI:
    
    • Goal is to have MRI in <24 hr
      
  • Diffusion-weighted imaging (DWI) is the most sensitive protocol for detection of tissue infarction
    
• Vascular imaging:
  
  • Either with initial imaging or inpatient workup, perform vascular imaging of the head and neck:
    
    • Almost 50% of patients with TIA have stenosis or occlusion of large arteries
      
  • Carotid duplex ultrasound can be used to detect internal carotid stenosis
    
  • CT angiography:
    
    • Can be performed at the time of initial noncontrast head CT
      
    • Can be used to detect stenosis in intracranial and extracranial vessels
      
    • Requires contrast
      
  • MR angiography:
    
    • Can be used to detect stenosis in intracranial and extracranial vessels
      
    • Time of flight (TOF) sequences can provide angiographic images without contrast