Focal neurologic deficits

(Redirected from Focal neurologic signs)

Background

  • Also known as focal neurologic signs
  • Refer to objective abnormalities of a specific region of the body detected on the neurologic examination

Focal Neurologic Signs Organized by Region

Brain

  • Frontal Lobe
    • Damage to the frontal lobe can lead to the following signs:
      • Sensorimotor deficit of the contralateral lower extremity
      • Language disturbances
      • Profound behavioral changes
      • Indifference, apathy
      • Disinhibition (labile and irritable)
      • Impaired judgement, decreased social graces
      • Akinesia (lack of spontaneous movements)
      • Impairment of memory
  • Parietal Lobe
    • Damage to the parietal lobe can lead to the following signs:
      • Agnosia
      • Anosognosia – Unawareness of a deficit
      • Unilateral spatial neglect (hemineglect)
      • Dyslexia, dysgraphia, dyscalculia
      • Impairment of tactile sensation
  • Temporal Lobe
    • Damage to the temporal lobe can lead to the following signs:
      • Upper homonymous quadrantanopsia
      • Cortical deafness
      • Wernicke’s aphasia (word deafness, auditory verbal agnosia)
      • Hallucinations
      • Complex partial seizures
      • Kluver-Bucy syndrome (Bilateral disease. Compulsion to attend all visual stimuli, hyperorality, hypersexuality, blunted emotional reactivity)
  • Occipital Lobe
    • Damage to the temporal lobe can lead to the following signs:
      • Contralateral homonymous hemianopia
      • Cortical blindness (bilateral lesions)
      • Visual hallucinations
      • Prosopagnosia
      • Alexia without agraphia
      • Loss of topographic memory and visual orientation
  • Limbic System
    • Damage to the limbic system can lead to the following signs:
      • Retrograde amnesia (long-term memory loss)
      • Anterograde amnesia (inability to form new memories)
      • Apathy
      • Loss of olfactory functions
      • Cerebellar
      • Damage to the cerebellum can lead to the following signs:
      • Ataxia of voluntary movements
      • Intention tremor
      • Dysarthria
      • Postural abnormalities
      • Hypotonia
      • Incoordination
      • Nystagmus, gaze paresis
  • Brainstem
    • Damage to the brainstem can lead to the following signs:
      • Crossed deficits – motor or sensory involvement of the face on one side of the body and the arm and leg on the other side
      • Cranial nerve palsies (see below)

Cranial nerves

  • CN I (Olfactory)
    • Anosmia + perceived change in taste of food
    • Deficit caused by shearing of the nerve ending passing through the cribriform plate usually by closed head trauma
  • CN II (Optic)
    • Monocular and binocular visual field defects
    • Monocular: Giant cell arteritis, Anterior ischemic optic neuropathy, glaucoma, optic neuritis, trauma, increased ICP, emboli/arteritis/stenosis leading to retinal ischemia, ophthalmic artery or vein occlusion
    • Binocular - Hemianopsia due to bilateral optic nerve disease.
  • CN III (Oculomotor) –See Third Nerve Palsy
  • CN IV (Trochlear)- See Trochlear nerve palsy
  • CN VI (Abducens)- See Abducens nerve palsy
  • Internuclear ophthalmoplegia - Lesion in medial longitudinal fasciculus, cannot adduct in horizontal lateral gaze, but normal convergence. Caused by multiple sclerosis or stroke
  • CN V (Trigeminal)
    • Jaw weakness and spasm. Jaw closure may be weak and/or asymmetric. +/- Trismus if irritative lesion to motor root.
    • See trigeminal neuralgia
  • CN VII (Facial)
  • CN VIII (Vestibular)
    • Dysfunction may be characterized by: tinnitus, deafness, nausea, vertigo, balance issues
    • See vertigo
  • CN IX (Glossopharyngeal)
    • Dysfunction may be characterized by: dysarthria, dysphagia
  • CN X (Vagus)
    • Dysfunction may be characterized by: hoarseness (unilateral vocal cord paralysis), dyspnea and inspiratory stridor (bilateral). Dysarthria, dysphagia.
  • CN XI (Accessory)
    • Dysfunction may be characterized by: Sternocleidomastoid and trapezius weakness leads to weak head rotation and shoulder shrug
  • CN XII (Hypoglossal)
    • Dysfunction may be characterized by: tongue deviation and wasting

Spinal Cord Syndromes

Peripheral nerve syndromes

  • Upper extremity
    • Ulnar
      • Cause of Injury: Elbow injury.
      • Sensory changes in the 5th and medial half of 4th digits, weak wrist flexors, “claw hand”
    • Radial
    • Median, distal
      • Cause of Injury: Wrist dislocation, laceration, Carpal Tunnel Syndrome
      • Weak flexion of radial half of digits and thumb, loss of abduction and opposition of thumb. Ape hand deformity, benediction sign. Loss of sensation of lateral three and one-half digits and nail beds
    • Median, proximal
    • Musculocutaneous
      • Cause of Injury: Anterior shoulder dislocation, entrapment due to hypertrophy
      • Elbow flexion and supination weakness, radial forearm sensory deficits
    • Axillary
  • Lower extremity
    • Femoral
      • Cause of Injury: Pubic rami fracture, pelvic fractures
      • Weak knee extension, anterior knee sensory deficits
    • Obturator
    • Posterior tibial
      • Cause of Injury: Knee dislocation
      • Weak toe flexion, plantar foot sensory deficit
    • Superficial peroneal
      • Cause of Injury: Fibular neck fracture, knee dislocation
      • Weak ankle eversion, lateral dorsal foot sensory deficits
    • Deep peroneal
      • Cause of Injury: Fibular neck fracture, compartment syndrome
      • Sensory deficit at dorsal 1st web space, weak ankle and toe dorsiflexion
    • Sciatic
      • Cause of Injury: Posterior hip dislocation
      • Lower leg weakness, foot drop, leg sensory deficits
    • Superior gluteal
    • Inferior gluteal
      • Cause of Injury: Acetabular pelvic fracture, s/p hip replacement
      • Abnormal gait, gluteus maximus weakness resulting in gluteus maximus lurch

Evaluation

Spinal cord tracts
Dermatomes and cutaneous nerves - anterior
Dermatomes and cutaneous nerves - posterior
Cutaneous innervation of the upper limb
Lower limb peripheral innervation

Management

  • Treat underlying condition

Disposition

  • Depending on cause

See Also

References

  1. LeBlond RF, Brown DD, Suneja M, Szot JF. LeBlond R.F., Brown D.D., Suneja M, Szot J.F. LeBlond, Richard F., et al. DeGowin’s Diagnostic Examination, 10e. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=1192&Sectionid=68670445. Accessed September 11, 2015.
  2. Waxman SG. Clinical Neuroanatomy, 27e. New York, NY: McGraw-Hill; 2013. http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=673&Sectionid=45395961. Accessed September 07, 2015.
  3. Ropper AH, Samuels MA, Klein JP. Adams & Victor's Principles of Neurology, 10e. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=690&Sectionid=50910870. Accessed September 07, 2015.
  4. Aminoff MJ, Greenberg DA, Simon RP. Disorders of Equilibrium. In: Aminoff MJ, Greenberg DA, Simon RP. eds. Clinical Neurology, 9e. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=1194&Sectionid=68656660. Accessed September 08, 2015.
  5. Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment Emergency Medicine, 7e. New York, NY: McGraw-Hill; 2011. http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=385&Sectionid=40357242. Accessed September 15, 2015.

Authors:

Ross Donaldson