{"id":5222,"date":"2011-07-14T20:24:33","date_gmt":"2011-07-14T20:24:33","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5222.htm\/"},"modified":"2011-10-07T01:35:12","modified_gmt":"2011-10-07T05:35:12","slug":"neuro-exam","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/neuro-exam.htm\/","title":{"rendered":"Neurological Exam"},"content":{"rendered":"

<\/span>Complete Neurologic Evaluation<\/span><\/h2>\n

<\/span>Mental Status<\/span><\/h3>\n

Alert, drowsy, stuporous (pt falls asleep during exam), comatose<\/p>\n

Lethargic-opens eyes, then falls back asleep<\/p>\n

Obtunded-moves your hand to noxious stimuli<\/p>\n

Stupor-general movement<\/p>\n

Coma-nothing<\/p>\n

 <\/p>\n

 <\/p>\n

GCS<\/p>\n

\"\"<\/a><\/p>\n

Orientation<\/p>\n

Optional:\u00a0 Serial 7s, Presidents, 3 objects, WORLD<\/p>\n

<\/span>Cranial Nerves<\/span><\/h3>\n

II<\/h4>\n

PERLA, Funduscopic Exam, VF (cut in half hemianopsia, homonymous or bitemporal or binasal)<\/p>\n

1.5 mm difference in pupils is physiologic anisicoria<\/p>\n

Papilledema-look for where vessels cross optic nerve margin, you should be able to see them sharp the whole way<\/p>\n

III, IV, VI<\/h4>\n

EOMI, Internucleur ophthalmoplegia, abnormal adduction of ipsilateral eye from MLF lesion<\/p>\n

III nerve palsy with preserved parasympathetics is usually from microvascular damage. If parasymp are down, think aneurysm<\/p>\n

V<\/h4>\n

Double Stim touch on face<\/p>\n

VII<\/h4>\n

Motor of face, can also have hyperacusis from loss of stapes dampening<\/p>\n

Weber:\u00a0 place a 512 hz fork in the center of the forehead.\u00a0 The ear with the conduction defect will hear the sound louder<\/p>\n

Rinne:\u00a0 if there is conduction defect, the sound will be louder on bone than air.\u00a0 Go back and forth between bone and air instead of waiting for bone to fade.<\/p>\n

VIII<\/h4>\n

Finger rubbing<\/p>\n

IX & X<\/h4>\n

Symmetry of palatal elevation and gag.<\/p>\n

XI<\/h4>\n

Head turn or shoulder shrug<\/p>\n

XII<\/h4>\n

Tongue points away from supranucleur lesion<\/p>\n

<\/span>Motor<\/span><\/h3>\n

Tone<\/p>\n

Tremor + rigidity=cogwheeling, spasticity=velocity dependant increase in tone,<\/p>\n

Power<\/p>\n

0-no contraction, 1-contraction without movement, 2-partial movement c gravity eliminated, 3-movement against gravity, 4-resistance can be given, 5-normal<\/p>\n

Pronater Drift and Gait with heels and toes and tandem<\/p>\n

Coordination<\/p>\n

Romberg<\/p>\n

Intention tremor from cerebellar lesions, test c finger to nose<\/p>\n

Dysdiadochokinesia-impairment of RAM<\/p>\n

Abnormal Movements<\/p>\n

Bradykinesia-decrease in normal spontaneous movements<\/p>\n

Akinetic Mutism-extreme lack of movement or interaction<\/p>\n

Catatonic mutism-same from schizo, may also have waxy flexibility<\/p>\n

Dyskinesia-tardives is choreoathetoid movements of face or trunk<\/p>\n

Choreiform-rapid movements, Athetoid-slower snake like<\/p>\n

Akathisia-can not sit still<\/p>\n

Most sensitive tests of corticospinal function is impairment of fine finger motions (tap forefinger and thumb) or rapid repeating hand movements<\/p>\n

<\/span>Reflexes<\/span><\/h3>\n

Frontal Release-glabellar, snout, root, grasp, palmomental reflexes indicate B frontal disease<\/p>\n

Hoffmann\u0092s sign-clonus of upper extremity, flexion of thumb with tapping of fingers<\/p>\n

<\/span>Sensory<\/span><\/h3>\n

DSS (double simulataneous stimulation)<\/p>\n

<\/span>Exam Notation<\/span><\/h3>\n

Mental Status:\u00a0 Ox4, alert, appropriate affect, digits 6#\u00ab, presidents \u00d6, 3\/3 5 min, proverbs, serial 7s<\/p>\n

CN:\u00a0 II-XII intact (PERRLA, EOMI, Face\/Gag\/Palate symmetrical, V1-3 normal) fundi \u0096<\/p>\n

Motor:\u00a0 Strengh 5\/5, normal tone\/bulk, no drift, F to N \u00d6, gait heel, toe, tandem normal, H to S normal<\/p>\n

Sensory:\u00a0 vibration, pain, touch, temp, position<\/p>\n

DTR:\u00a0 draw picture<\/p>\n

 <\/p>\n

<\/span>NeuroOptho<\/span><\/h2>\n

monoocular diplopia or vision loss = eye or optic nerve problem<\/p>\n

 <\/p>\n

3rd nerve palsy-Eye ptosis, down & out, dilated pupil is a complete 3rd. These patients need an arterial study for aneurysm immediately<\/p>\n

 <\/p>\n

Pupil sparing=infarction, 75% diabetes 25% arthritidies. not emergent<\/p>\n

 <\/p>\n

VI is the longest course, sensitive to external compression<\/p>\n

 <\/p>\n

No such thing as a motor-sparing 3rd, must be intrinsic eye problem<\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>The Rapid EM Neuro Exam:<\/span><\/h2>\n

Henry’s law:\u00a0 hear them talk, see them walk, look at their eyes.<\/p>\n

Orientation is always lost in the same order if from organic disease:<\/p>\n

    \n
  1. Time and Date<\/li>\n
  2. Specific Place<\/li>\n<\/ol>\n

    Dividing line of disease<\/p>\n

      \n
    1. General Place<\/li>\n
    2. Name (Self)<\/li>\n<\/ol>\n

      Well cadenced, rapid speech=functioning cortex.<\/p>\n

      Ask if helicopters eat their young for hardware vs. software discrimination<\/p>\n

       <\/p>\n

      Have pt close eyes and put their right thumb on their left ear and then stick out their tongue.<\/p>\n

      Facial asymmetry takes place below the nose, observe the nasolabial fold.\u00a0 Have patient swallow.\u00a0 If they are speaking to you clearly, there is no hypoglossal defect.<\/p>\n

      Pronater drift:\u00a0 test for 15 seconds.\u00a0 can not drop arm without pronation to be real weakness.\u00a0 Have patient close eyes, if random movements of the arms and fingers, indicates non-dominant parietal lobe dysfunction.\u00a0 Won’t hold arm up at all, motor impersistance=frontal lobe disease.<\/p>\n

      Reflexes:<\/p>\n

      S1S2=Ankle<\/p>\n

      L3L4=Knee<\/p>\n

      C5C6=Wrist\/Hand<\/p>\n

      C7C8=elbow<\/p>\n

      note, no L5 reflex so you must have patient extend their big toe.<\/p>\n

       <\/p>\n

      Rooting, snooting, grasping, sucking are frontal release signs.<\/p>\n

       <\/p>\n

      Columbus award:\u00a0 when you don’t know where you are going, where you are, or where you have been.<\/p>\n

       <\/p>\n

      <\/span>Exam on Coma Patients<\/span><\/h2>\n

      <\/span>Dolls’ Eyes<\/span><\/h3>\n

      Oculocephalic reflex or Cervico-ocular reflex<\/p>\n

       <\/p>\n

      In normal, alert man, this brain-stem reflex is inhibited by gaze control mechanisms. The eyes go wherever the cortex wants them to go.<\/p>\n

       <\/p>\n

      In the comatose patient, this inhibition is lost, and the oculocephalic reflex becomes disinhibited, and clinically demonstrable.\u00a0 Therefore, the eyes deviate in the direction opposite the head turning.\u00a0 This is a positive Dolls’ eyes response. Eyes stay focused on whatever they were looking at before head turning.<\/p>\n

       <\/p>\n

      The brain stem has to be intact to (1) receive the afferent input of the neck stretch receptors and\/or the vestibular system; (2) feed<\/p>\n

      that information to the abducens nuclei (which manage unconscious eye movements, as opposed to the pontine paramedian reticular formation, which<\/p>\n

      coordinates conscious horizontal conjugate gaze); (3) send a signal to the ipsilateral lateral rectus to abduct that eye; (4) transmit the information across the midline to the contralateral median longitudinal fasciculus, whence it goes to the horizontal component of the third nerve nucleus and<\/p>\n

      out the third nerve to adduct the contralateral eye.\u00a0 When you demonstrate that this reflex works in both directions, you have shown that the parts of the brainstem required to drive the cortex are intact.\u00a0\u00a0 This means that coma is not due to a brainstem lesion but rather something higher, usually bilateral hemispheral dysfunction, rarely the diencephalon alone.\u00a0 QED. (cf. Parvizi J, Damasio AR.\u00a0 Neuroanatomical correlates of brainstem coma. Brain 2003;126:1524-1536).<\/p>\n

       <\/p>\n

      Based on antique dolls that would look forward when you turn their head.<\/p>\n

       <\/p>\n

      present normally, the eyes stay fixed forward c head movement, abnormal they are absent, move c head<\/p>\n

       <\/p>\n

      Roberts TA, Jenkyn LR, Reeves AG. Arch Neurol 1984;41:1242-3. On the notion of doll’s eyes Buettner UW, Zee DS. Vestibular testing in comatose patients. Arch Neurol1989;46:561-3<\/p>\n

      <\/span>Calorics<\/span><\/h3>\n

      10 cc ice water, place head 30 degrees above supine.\u00a0 Slow away, then rapid back to midline.\u00a0 If no rapid=cerebral damage.\u00a0 Response named for rapid component<\/p>\n

       <\/p>\n

      <\/span>Glasgow Coma Scale<\/span><\/h3>\n

      Points<\/strong> Best Eye Opening<\/strong> Best Verbal Response<\/strong> Best Motor Response<\/strong>6 – – Obeys 5 – Oriented Localizes pain 4 Spontaneous Confused Withdraws to pain 3 To speech Inappropriate Flexor (decorticate) 2 To pain Incomprehensible Extensor (decerebrate) 1 None None None The Glasgow Coma Scale score is determined by adding the values for eye opening, verbal response, and motor response. Possible values range from 3 to 15. Note that this scale rates the best response only. In patients who are intubated, in whom assessment of best verbal response cannot be performed, notation of this is made in the Glasgow Coma Scale score by adding a “t” to the end of the score. In patients who are intubated, the best possible score would therefore be 11t. Certain numerical values of the Glasgow Coma Scale have particular clinical significance. Patients with a Glasgow Coma Scale of 7 or less are considered to be comatose. Patients with a Glasgow Coma Scale score of 8 or less are considered to have suffered a severe head injury.<\/p>\n

       <\/p>\n

      \"\"<\/a>\"\"<\/a><\/p>\n

      If not obeying commands- press on the supra-orbital nerve to inflict pain. If the either one hand reaches above the clavicle that scores 5 ie: localizing to pain. If the hand does not come above the clavicles but is moving towards the head, score 4 for normal flexion. If the response is a clenched fist with a flexed wrist and elbow, as in decorticate posturing, score 3. If the patient extends the elbow and flexes a clenched wrist, that is extension to pain and decerebrate posturing scoring 2. And of course no response scores 1. Pressing on nail folds is not informative as you do not know if the patient is localizing (5)or normal flexing \/ withdrawing (4) to pain. Besides, if that arm is paralyzed or lacks sensation secondary to a peripheral nerve injury you may misjudge the GCS. (Narani)<\/p>\n

      A topic close to my heart. GCS is often very poorly assessed, and interindividual difference can be spectacular. It fascinates me to see a previously stable GCS suddenly change by a number of units at the time of a nursing shift handover! A. Central pain needs to be central and specific. By far the best is the supraorbital nerve. Another reasonable site is a trapezius squeeze. The ‘sternal rub’ is useless, non specific and also disfiguring (how many times have you seen bruising after too many people have done misguided, violent sternal rubs). I threaten to break the arms of any of my own staff I see doing it. Attached find a picture of a patient who had one too many vigorous sternal rubs. The supraorbital nerve is also the only specific way to distinguish between appropriate (M4) and inappropriate flexion (M3) and localisation (M5), depending on whether the hand comes ABOVE the clavicle [need to come above the clavicle to score a 5] B. It is part of your overall neurological assessment of a patient, which includes an examination to rule out spinal cord injury. I have attached the original description of the motor response from Teasdale and Jennett. C. Hourly \/ 4th hourly GCS is of much less value in a sedated patient. One of the standard ‘errors’ in APACHE II scoring is to assign a GCS3 to someone deeply sedated and unresponsive (=12 points instantly!). A great way to dishonestly bring down your SMR and one thing I specifically look at when assessing a unit’s data during training accreditation inspections. I note your question refers to ongoing GCS assessments in ICU – that is a different animal to a one off assessment in the emergency department, and the reproducibility of ICU observations is paramount (rather than the ‘best’ response per se) Cheers, Ian Ian Seppelt FANZCA FJFICM<\/p>\n

       <\/p>\n

       <\/p>\n

      Thomas Bleck<\/strong> <tbleck@gmail.com<\/a>> Posturing or localization in response to any noxious stimulus, face or trunk or extremities, provides important information on what parts of the brainstem are working (flexion = rubrospinal system in control of the spinal cord, extension = vestibulospinal system in control, no arm movement but knee flexion, medullary centers still working after vestibular efferents lost). \u00a0 As I mentioned before, there are occasional patients who do nothing in response to nailbed pressure but who extend, flex, or even localize with a sternal rub. \u00a0So while I don’t do a sternal rub if I get a reproducible response to nailbed pressure in a comatose patient, I do perform the sternal rub if other stimuli below the neck have not elicited anything.<\/p>\n

       <\/p>\n

      <\/span>Adie’s Pupil<\/span><\/h2>\n

      Classically, the affected pupil will be larger than the fellow eye, and exhibit a sluggish reaction to light. The pupil will react vigorously to near stimuli but the near response is tonic, meaning the miosis persists longer in the affected eye with slow redilation after removal of the near stimulus. Adie’s pupil is most often found in young women and is associated with a generalized loss of deep tendon reflexes.\u00a0 Frequently, patellar and Achilles reflexes are absent.\u00a0 There is a feeling that light is too bright in the affected eye (because the pupil helps to reduce light intensity by constricting in bright light). The condition is believed to result from damage to the cilliary ganglion caused by infectious (viral) or vascular disease. Adie’s pupil is supersensitive to dilute solutions of pilocarpine and can be positively identified if 1\/8% pilocarpine constricts the pupil (this will not constrict a normal pupil, such as in the patient with a third cranial nerve palsy as the etiology of anisocoria).\u00a0 (Emedhome.com)<\/p>\n

       <\/p>\n

      Quick Motor Exam<\/p>\n

      Tone<\/p>\n

      Pronator Drift<\/p>\n

      F to N<\/p>\n

      Fine Finger Motion<\/p>\n

      Hand Bulk<\/p>\n

      Finger Extensor strength and intrinsic muscle strength of finger spread<\/p>\n

       <\/p>\n

      <\/span>Babinski<\/span><\/h2>\n

      not sensitive and its LRs make it fairly useless. Speed of foot tapping is more demonstrative of UMN lesion. Slowed foot is sign of the lesion. (Neurology Volume 65(8), 25 October 2005, pp 1165-1168)<\/p>\n

       <\/p>\n

      <\/span>Ptosis<\/span><\/h2>\n

      To examine the levator palpebrae muscle, note is made of the portion of the iris that is covered by the upper lid, and compared with the opposite side. Ptosis can be exaggerated by having the patient look up. If ptosis is present, the patient should be tested for lid fatigue: the ptosis may worsen when the patient refrains from blinking for a time or attempts to maintain upgaze. Ptosis from myasthenia gravis is often asymmetric, fatigable, and improves with short periods of rest (4). Other conditions causing ptosis include Horner’s syndrome, botulism (or injection of botulinum toxin), palpebral trauma, and cluster headache; ptosis also may be congenital (5). \u0093Pseudoptosis\u0094 is caused by enopthalmos (e.g., from an orbital blowout fracture), which makes the lid seem to be relatively lower on the side with the sunken globe. (JEM 2008)<\/p>\n

       <\/p>\n

      <\/span>The Brainstem from Life in the Fast Lane & Chris Nickson<\/span><\/h2>\n

      Brainstem Rules of 4<\/p>\n

      11<\/a><\/p>\n

      \u00a0Share<\/a><\/p>\n

      Hands up who enjoyed learning the anatomy of the brainstem in medical school?<\/p>\n

      Hmm, thought so.<\/p>\n

      \"brainstem<\/a><\/p>\n

      In 2005, Peter Gates published a superb paper titled:<\/p>\n

      \u0091The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non-neurologist\u0092.<\/p><\/blockquote>\n

      Gates described a simplified method for answering the question \u0091Where is the lesion?\u0092 using only the parts of the brainstem that we actually examine during a clinical examination to understand brainstem vascular syndromes.<\/p>\n

      Firstly, a quick review of the blood supply of the brainstem. Simply put the blood supply comes from:<\/p>\n

        \n
      1. paramedian branches<\/li>\n
      2. long circumferential branches (SAP)<\/li>\n<\/ol>\n
        \n