This is an important clinical distinction to make, but may not always be easy. 

Myopathy (Break down or inflammation of muscle) 

  • Tends to affect (large) muscle groups (i.e Hips, Shoulders) causing proximal weakness.
  • There will be a lack of sensory deficits (but they may complain of myalgias or tenderness to palpation (if myositis)). 
  • Reflexes should be intact and no fasciculations should be seen. 

Neuropathy (Damage to your peripheral nerves)

  • Tends to affect distal muscles first in a length dependent distribution. 
  • Typically will have sensory findings (i.e paresthesia, dysesthesia).
  • May have loss of reflexes (i.e Lower Motor Neuron pathology).
  • Fasciculations may be present.

NOTE: Tests such as CK and NCS/EMG can help delineate the two etiologies should the clinical picture not be clear. 


  1. Saguil A. Evaluation of the patient with muscle weakness. Am Fam Physician. 2005 Apr 1;71(7):1327-36.
  2. Paganoni, S., Amato, A. Electrodiagnostic Evaluation of Myopathies. Phys Med Rehabil Clin N Am. 24 (2013) 193–207.
  3. Chawla, J. Stepwise Approach to Myopathy in Systemic Disease. Front Neurol. 2011; 2: 49.


Rinne and Weber testing are useful clinical bedside assessments to

differentiate the two primary causes of hearing loss.

RINNE (+): Air conduction > Bone Conduction [Normal or Sensorineural hearing loss]

RINNE (-): Bone Conduction > Air conduction [Conductive hearing loss] 



  • Lateralizes to better ear in Sensorineural hearing loss
  • Lateralizes to worse ear in Conductive hearing loss
Credit: Clinical Neurology, 10e, 2017


  1. Clinical Neurology, 10e, 2017. Neurologic History & Examination. Roger P. Simon, Michael J. Aminoff, David A. Greenberg

Pronator Drift is commonly assessed during a stroke assessment. It is a marker of upper motor neuron weakness.


In upper motor neuron weakness, pronation is stronger than supination in the upper extremities, causing a pronation of the affected arm. See Video.

NOTE: This test can be useful in determining consistency. If a patient’s weakness is functional, the patient will almost always drop their arm without pronating it.

Credit: Epomedicine


  1. Clinical Neurology, 10e, 2017. Neurologic History & Examination. Roger P. Simon, Michael J. Aminoff, David A. Greenberg

Classical findings of Normal Pressure Hydrocephalus (NPH) include:

  1. Ataxia (typically the initial and most prominent symptom of NPH)
  2. Dementia
  3. Urinary Incontinence (typically appears late in the illness)

Abnormal accumulation of cerebrospinal fluid (CSF) gradually dilates the lateral ventricles of the brain. The gradual nature of ventriculomegaly allows for the CSF pressure to adapt and remain normal, hence normal pressure hydrocephalus.

CSF accumulation in the lateral ventricles puts pressure on adjacent cortical tissue and results in the triad listed above.


  1. Verrees M, Selman WR. Management of normal pressure hydrocephalus [summary for patients in Am Fam Physician. 2004;70(6):1085-1086]. Am Fam Physician. 2004;70(6):1071-1078.
  2. McGirt MJ, Woodworth G, Coon AL, et al. Diagnosis, treatment, and analysis of long-term outcomes in idiopathic normal-pressure hydrocephalus. Neurosurgery. 2005;57(4):699-705; discussion 699-705.

Anterior cord syndrome arises from damage to the spinothalamic and corticospinal pathways. 

Occurs due to injury of the anterior spinal artery (ASA) affecting the anterior two-thirds of the spinal cord.

The anterior spinal artery (ASA) is the amalgamation of the vertebral arteries with co-lateral blood flow from several radicular arteries (the artery of Adamkiewicz is the most important of these!). This leaves multiple areas of the cord vulnerable to watershed ischemia.

The spinal cord receives blood supply from two posterior arteries (25%) and one anterior spinal artery (75%)

This damage manifests as:

Loss of motor function (flaccid paralysis), pain and temperature/ sensation loss distal to the lesion.

***Only vibration, position, and tactile sensation are preserved (as posterior column remains intact).

Potential causes:

  1. C-spine injury
  2. Thrombosis causing ischemic injury to ASA
  3. Anterior cord compression from extrinsic mass 
  4. Aortic dissection or hypotension
  5. AAA repair [stats]

NOTE: The overall prognosis for recovery of function is poor.


  1. Steven Go. Chapter 258: Spine Trauma. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e
  2. Grecu L, Schonberger RB. Vascular Disease In: Barash PG, Cullen BF, Stoelting RK, Cahalan M, Stock MC, eds. Clinical Anesthesia, 6th ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2009: Ch. 8.
  3. Foo, D; Rossier, AB (Feb 1983). “Anterior spinal artery syndrome and its natural history.”. Paraplegia. 21 (1): 1–10.
  4. Norris EJ. Anesthesia for Vascular Surgery. In: Miller RD, Eriksson LI, Fleisher L, Wiener-Kronish JP, Cohen NH. Miller’s Anesthesia, 8th ed. Philadelphia, PA: Elsevier Saunders; 2014: Ch. 69

The Caloric Reflex Test is used to test the Vestibulo–ocular reflex. It is one of the tests used to assess for brain stem death.


Cold (= or >30C) or warm water (= or > 44C) is flushed into the external auditory canal via a clean syringe. The difference in temperature between the water and your body generates convection signals in the endolymph of the ear mimicking head rotation. 

Mnemonic= COWS

The most common way to remember the normal response is COWS (used to remember the fast beating nystagmus response) in awake, normal subjects.

Irrigated with COLD water: Eyes deviate to ipsilateral (same-sided) ear and the nystagmus beats away to the OPPOSITE ear.

Irrigated with WARM water: Eyes deviate to contralateral (opposing-sided) ear and the nystagmus beats towards to the SAME ear.





An Excellent video that demonstrates the effect of cold water irrigation on an awake/ normal individual.

NOTE: In comatose patients, the nystagmus phase will not be present, only the conjugate eye deviation.

With brain stem damage the eyes remain mid line and the vestibular responses are abolished (or altered, depending on the severity of the lesion) SEE BELOW.

(MLF; note that irrigation in this case results in lateral movement of the eye only on the less active side) Img Cred: Neuroscience 3rd Edition.
(MLF; note that irrigation in this case results in lateral movement of the eye only on the less active side)
Img Cred: Neuroscience 3rd Edition.


  1. Webb C. COWS caloric test. Ann Emerg Med. 1985 Sep;14(9):938.
  2. Oculocephalic and Cold Caloric Reflexes (CN III, IV, VI and VIII).
  3. Purves, Dale et al. NEUROSCIENCE: Third Edition. Sunderland, MA: Sinauer Associates, Inc., 2004. Print.


Classical clinical symptoms of Wernicke’s Encephalopathy:

  • Encephalopathy (i.e disorientation, inattentiveness)
  • Oculomotor dysfunction (i.e typically bilateral horizontal nystagmus, lateral rectus palsy)
  • Gait ataxia (May appear wide-based and slow)


  1. Victor, M, Adams, RA, Collins, GH. The Wernicke-Korsakoff syndrome and related disorders due to alcoholism and malnutrition. FA Davis, Philadelphia 1989.
  2. Chapter 8: Disorders of Equilibrium. Clinical Neurology, 9e

Classical clinical symptoms of Lewy Body Dementia (LBD) include:

  1. Fluctuating level of cognitive impairment
  2. Recurring visual hallucinations
  3. Parkinsonism (i.e bradykinesia, rigidity, tremor)


  1. Fernandez HH, Wu CK, Ott BR. Pharmacotherapy of dementia with Lewy bodies. Expert Opin Pharmacother. 2003 Nov;4(11):2027-37.
  2. Chapter 448: Alzheimer’s Disease and Other Dementias. William W. Seeley; Bruce L. Miller. Harrison’s Principles of Internal Medicine, 19e

Neuroleptic medications can produce hyperprolactinemia even at very low doses and are the most common cause of galactorrhea in dopamine-receptors-blockedpsychiatric patients.


Hyperprolactinemia with neuroleptic use is secondary to the blockade of dopamine receptors with these drugs. (Dopamine normally inhibits prolactin, and with dopamine’s blockade, hyperprolactinemia can result.) Amenorrhea and galactorrhea are the main symptoms of hyperprolactinemia in women, and impotence is the main symptom in men, although men can also develop gynecomastia and galactorrhea.

NOTE: Other causes of hyperprolactinemia include severe systemic illness such as cirrhosis or renal failure, pituitary tumors, idiopathic sources, and pregnancy.


  1. Kleinberg DL, Davis JM, de Coster R, Van Baelen B, Brecher M. Prolactin levels and adverse events in patients treated with risperidone. J Clin Psychopharmacol 1999;19:57-61
  2. Wudarsky M, Nicolson R, Hamburger SD, Spechler L, Gochman P, Bedwell J, Lenane MC, Rapoport JL. Elevated prolactin in pediatric patients on typical and atypical antipsychotics. J Child Adolesc Psychopharmacol 1999;9:239-45

Myasthenia Gravis


  • Auto-antibodies against ACh Receptor
  • POST-synaptic
  • Motor response decreases with successive contractions of voluntary skeletal muscles (particularly ocular, masticatory, facial, deglutition, lingual) WATCH for resp muscle weakness!
  • TENDON reflexes are maintained
  • EMG: a typical decremental response on repetitive stimulation
  • Smooth and cardiac muscle are not involved and other neural functions are typically preserved (NO autonomic dysfunction)
  • Thymectomy is an important treatment option for MG (associated with thymoma and thymic hyperplasia)
  • Atrophy/Pain are typically not reported


  • Auto-antibodies against Ca+ channels
  • PRE-synaptic
  • Motor response improves with successive contractions., e.g. improvement of power on repeated hand grip (a phenomenon known as “Lambert’s sign“)
  • At rest, reflexes are typically reduced; with muscle use, reflex strength increases
  • The pupillary light reflex may be sluggish
  • Sometimes causes autonomic (involuntary) symptoms such as dry mouth, constipation, impotence and bladder urgency
  • Lambert-Eaton may be regarded as a paraneoplastic syndrome (60% of LEM have Small cell lung cancer, but only 3% of SCLC experience LEM)


  1. 461: Myasthenia Gravis and Other Diseases of the Neuromuscular Junction. Daniel B. Drachman; Anthony A. Amato. Harrison’s Principles of Internal Medicine, 19e
  2. Engel  AG, ed. Neuromuscular Junction Disorders. Handbook of Clinical Neurology. Vol 91. Amsterdam: Elsevier; 2008.
  3. Jayawant  S, Parr  J, Vincent  A. Autoimmune myasthenia gravis. Handb Clin Neurol. 2013;113:1465–1468.