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Great for a med school neurology rotation. I love how this book series is more in depth than some other clerkship books but it still is a fairly easy read. I really. Blueprints: Neurology. Pages · (zlibraryexau2g3p_onion).pdf Born a Crime Blueprint Reading: Construction Drawings for the Building Trades. Blueprints Neurology provides students with a complete review of the key topics and concepts—perfect for clerkship rotations and the USMLE.

Make sure that true weakness is the complaint. Use laboratory and electrophysiologic tests wisely. Pattern of Weakness Below. Individual diseases in each category predominantly in proximal muscles. Are they consistent with your localization? It is useful to consider the disorders that cause weak- ness in an anatomic order. Associated signs and symptoms may occasionally Associated Signs and Symptoms include muscle pain if the muscle disorder is inflam- matory.

Some NMJ disorders A lesion involving a particular peripheral nerve will can lead to ptosis as well as weakness of extraocular. Reflexes are characteristi. Differential Diagnosis Differential Diagnosis Primary muscle disorders. NMJ disorders is not the pattern of weakness.

Some NMJ disorders may have associated muscles are nearly paralyzed. Distal muscles are affected later or not as change from hour to hour. NMJ problems. Disorders affecting a single peripheral nerve are ever. Some of the diseases in this category have EMG can help confirm a primary muscle disorder. Certain systemic. The characteristic feature of nerve while sparing other. Depending on the specific severely. The demon. NMJ disorders.

Laboratory Studies Laboratory Studies Some disorders of muscle are characterized by an ele. By their nature. The degree of weakness may known as mononeuropathies. Differential Diagnosis neuropathy. Mononeuropathy multiplex is associated with systemic vasculitis and other metabolic or rheumatologic dis- eases. Mononeuropathies most commonly occur as a result ropathy usually appears first in the distal muscles. Peripheral nerve disorders are discussed in Chapter Biceps C5 L2. Polyradiculopathies are often inflamma- nantly innervated by fibers from one nerve root see tory or infectious.

These disorders are discussed in Table In the leg. Put sim- ply. Pattern of Weakness The intricacies of brachial and lumbosacral plexus Laboratory Studies anatomy Fig.

Differential Diagnosis tiple different muscles. Pattern of Weakness Single radiculopathies usually require MRI of the spine to rule out structural causes. Objective sensory loss is rare in disorders affecting a single nerve root because there is overlap from neigh- boring roots. The result is that most muscles Single radiculopathies can be caused by herniated discs are innervated by fibers that originate from more than or by reactivation of varicella-zoster virus shingles.

In any case. Spinal cord disorders are discussed in Chapter MRI of the brachial plexus or pelvis or descending corticospinal tracts. They are discussed in Chapter Bladder and bowel incontinence may occur. There may be a sensory level loss of sensation rhage. Spinal cord disorders cause weakness in two ways.

This weakness occurs lumbosacral plexus may be necessary to rule out in an upper motor neuron UMN pattern Fig. Diabetic patients are prone to develop a character- Typically. T1 Radial nerves. Lesions in the base of the pons may lead to weak- ness of the ipsilateral face and contralateral arm and leg crossed signs. Knowledge of the homunculus of the motor all of the potential etiologies in this category.

The strip Fig. Associated Signs and Symptoms more lateral lesions lead primarily to face and arm Lesions of the cerebral hemispheres frequently have weakness. Imaging of the brain is important to evaluate almost Chapter Deep hemispheric lesions.

Amyotrophic lateral sclerosis causes degeneration of both the corti- cospinal tracts and anterior horn cells. Left hemispheric lesions may cause apha. The common characteristic in all is the fibers more medially. The STT and the trigeminal tract distribution of symptoms. Fine sensory discrimination and localization of pain. The diagnosis of these problems includes Facial sensation is carried to the brainstem by the analysis of the nature. The medial fibers are from the information to the CNS.

Axons from these nuclei cross at strate sensory abnormalities in a patient with sensory the lower medulla to form the medial lemniscus symptoms. At the level of the spinal cial senses: The evaluation of vibration. In some instances. Information the lowest area and the leg in the parasagittal area. At the level of Somatosensory abnormalities may be character.

Blueprints in Neurology

Whatever the situa- There is a somatotopic arrangement of fibers in tion. From here. Pain and temperature functioning of the sensory cortex. Proprioception malities: The next step is to record the sensory abnormali- using a very soft stimulus. The following list defines some and asking the patient to indicate the direction of of the terminology used to describe sensory abnor- movement test joint position sense.

It is important to reg- with a pin. Pain sensation is tested ties using accepted definitions. Thermal modalities are tested using ob. Moving the great toe up and down should be recorded.

The testing of vibration sense requires a dles. Touch sensation is tested with a wisp of cotton. Parietal stroke.

This stimuli. The opposite is hypesthesia. Distal muscle weakness. Sensory dysfunction becomes manifest through two matomes involved but preservation of posterior types of symptoms: Posterior circulation strokes. Spinal cord Sensory level: Peroneal neuropathy. This table provides a guide to the field cuts. Central sensory loss involving the tha. In brain. Spinal cord disease leads to a characteris. They are In a patient complaining of sensory disturbances.

Although in theory it is easy to distinguish peripheral nerve from segmental nerve or root. Sometimes the sensory problems accompany tion of the respective neurologic problem are repre- other symptoms—such as weakness.

There are many pri- usually means disruption of nerve excitation. The former malities is to establish the cause. Blood supply to the inner ear is via the internal Labyrinthine concussion may result from head the brain appears to habituate to slow changes.

Infarction of the labyrinth. A determination should also be made as to lum. Patients develop a sudden and spontaneous onset of vertigo. Neither ally rotatory but may be linear. The neurologic ab. A injury irrespective of whether there is an associated useful approach Box to sorting out the etiology skull fracture. Nystagmus is strictly unilateral right vestibular systems. Vertigo is vertigo. Vestibular neuronitis presents as an acute unilat- normalities responsible for this symptom are outlined eral complete or incomplete peripheral vestibu- in detail in Chapter 8.

Complete recovery may not imbalance of neural activity between the left and occur for months. Vertigo is sometimes accompanied by is to determine the periodicity and duration of the hearing loss and tinnitus. Dysequilibrium is a sensation of imbalance or Unidirectional nystagmus may arise from either cen- unsteadiness that is usually referable to the legs rather tral or peripheral dysfunction.

The blood supply to the central and peripheral whether the vertigo is of peripheral or central origin.. Light-headedness of these latter features. The designation neuronitis is inaccurate simply cannot define their symptoms accurately. Tinnitus or hearing loss suggests a peripheral tery. Broadly speaking. Recovery symmetric bilateral loss of vestibular function as represents central compensation for the loss of pe- with ototoxic drugs or from a slow unilateral loss of ripheral vestibular function.

Accompanying nausea and vomiting clude vertigo. Vertical and direction-changing two categories. This chapter focuses on these source of the vertigo. Vertigo does not result from and may be suppressed by visual fixation.

The attacks are brief. Observers may note that.

The offending ear is the one Benign positional paroxysmal vertigo BPPV that is toward the ground when vertigo occurs during Central the test. Prior to losing consciousness. Perilymph fistula once the head comes to rest. Diagnosis is estab- Positional vertigo lished by demonstrating the characteristic downbeat- ing and torsional nystagmus with the Dix-Hallpike Peripheral test Fig.

The illustration bellar artery. Lateral medullary or cerebellar infarction When the head is stationary. Patients with benign positional paroxysmal ver.

A perilymph fistula results from disruption of the lining of the endolymphatic system. With head movements. Brainstem or cerebellar stroke is the most impor- tant differential diagnosis in patients with suspected acute vestibular neuronitis.

The head is turned in auditory artery. There may be asso- Spontaneous vertigo ciated severe nausea and vomiting. Attacks occur most frequently Vertigo when the individual is reclining in bed at night or upon awakening in the morning. A central-type nystagmus from acute unilateral vestibular dysfunction. Attacks may Single prolonged episode occur in clusters.

This is followed Syncope is a transient loss of consciousness and pos- by the abrupt onset of vertigo. Infarction of the inner ear presents with demonstrates treatment for BPPV originating from a sudden onset of deafness. It is caused by an typical of benign positional paroxysmal vertigo.

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A positioning Epley maneuver Fig. BPPV results from freely moving crystals of cal- Labyrinthine concussion cium carbonate within one of the semicircular canals. The Epley positioning maneuver begins with the positioning used for the Dix-Hallpike maneuver and continues with a series of other positions.

Less commonly. There are essentially two neurologic varieties of syn- cope. The examiner looks for a rotatory and down-beating nystagmus. Afferent impulses to cardiac causes. Syncope is charges from arterial including cardiac or great ves- most commonly a manifestation of hypotension due sel or visceral mechanoreceptors. Cardiac causes include asystole. Reproduced with permission of the Department of Neurology. Humbolt University.

Its pathophysiology Vasovagal syncope Strong emotions or acute pain involves a reflex triggered by excessive afferent dis-. The more common is neurogenic syn. Excessive vasodilation usually has a neurologic cause. Low intravascular volume can result from Autonomic failure is characterized by an inability dehydration.

Type of Syncope Pathophysiologic Trigger cope. Different terms are used to describe this obstruction. If a neurologic cause for syncope is sus. If a car. If release norepinephrine on standing. An echocardiogram is indicated if a neurogenic syncope and autonomic failure central or peripheral. The underlying pathologic hypotension or syncope. Beta blockers a sudden change in posture or prolonged standing. A variety of hallmark of both is the failure to release norepineph.

In evaluating patients with syncope or orthostatic hypotension. Patients usually complain of light. The vermis bears the brunt of the damage. It is also helpful presentation. Hence it is appropriate to distinguish cerebellar ataxia from Cerebellar hemorrhage or infarction typically pre- sensory ataxia.

Associated symptoms ited chance of improvement.

Cerebellar stroke should be considered a med- only process that may underlie a gait disorder. A limited differential diagnosis nied by an alcoholic polyneuropathy.

Vermal lesions typically pro. The details of a few of these mentation of nutrition offer the best although lim- disorders are specified below. Hemispheric between the ages of 2 and 7 and usually follows a Postinfectious cerebellitis typically affects children duce prominent truncal and gait ataxia. A classification based on this approach weeks or months.

It is important. Ataxia is not the stem. Level of arousal may be depressed rate. Cessation of drinking and supple- is outlined in Box Alcohol is the can often be generated by considering the acuity with most common cause of acquired cerebellar degenera- which symptoms begin and whether the disorder is tion. Vitamin E deficiency clusion.

The disease usu. Truncal ataxia: Impaired control of truncal posture. Classic as- weeks and then stabilizes. Children present Autosomal recessive cerebellar degenerative with acute onset of limb and gait ataxia as well as disorders dysarthria. The illness lasts a few weeks and re. Creutzfeldt-Jakob disease complete inability to walk.

Abnormality of the range and force of a episodic course movement. PCD is typically associated with extensor plantar responses. Hypothyroidism derlying drug intoxication and for a mass lesion in the posterior fossa. A variety of autoanti. The episodic ataxia EA syndromes are characterized bodies e.

EA-1 is caused by mutations in a voltage-gated. Rhythmic side-to-side oscillations agents of the limb as it approaches the target Multiple sclerosis Dysdiadochokinesia: Broad-based and unsteady. The diagnosis is one of ex. MRI is usually normal..

Childhood metabolic disorders e. Slow scanning and monotonous speech Paraneoplastic cerebellar degeneration Nystagmus Alcoholic or nutritional cerebellar degeneration Chronic onset and progressive course Autosomal dominant spinocerebellar degenerations varicella or other viral infection. Severity ranges from mild unsteadiness to Infectious e. Wilson disease. Onset is usually in childhood.

Creutzfeldt-Jakob disease. Miller Fisher syndrome. Mild to moderate cognitive decline is a late feature in most of the spinocerebellar ataxias SCAs. Episodes are brief. Attacks drome. IgG anti-GQ1b anti- nystagmus. EA-2 is tive loss rather than to cerebellar dysfunction. SCA6 is allelic to EA The normal func. Associated neurologic ab- normalities e. The typical presentation is the vomiting and depressed level of consciousness insidious onset of progressive impairment of gait and suggests a cerebellar stroke.

Friedreich ataxia. The ataxia is due to propriocep- tack skeletal muscle myokymia is associated. There is often difficulty with gait initiation. These factors are not dis. With increasing severity. The patient advances with small. The following sections are devoted to de- scriptions of the different types of gait disorders. Posture is flexed. One difference in progressive ciently characteristic to permit identification of the supranuclear palsy is that posture tends toward exten- underlying disorder based solely on the features of sion rather than flexion.

The adductor tone is in- creased. The affected leg is stiff and does not flex at the hip. Gait initiation is impaired. The foregoing description is abnormalities. This is especially true in the elderly. During normal walking.. Postural reflexes are impaired. Not all gait disorders are the fling with small steps and reduced arm swing. The leg is circumducted. The arm is in one place without being able to move forward.

Gait is narrow-based. Another the opposite leg to rise and the trunk to tilt toward feature is that the patient may adopt extreme pos- the fixed leg. There is no single typical characteristic to this gait. Weakness of the abductors and con. With dle weakness. It is wide. Contact with the ground is tion. The circumduction characteristic of the genuine. The term astasia- side during walking. The examiner seeks signs of frontal lobe providing the volitional control of micturition.

As the bladder becomes distended. It is important to cuits act as on-off switches to shift the lower urinary obtain information about initiation. The M region projects to the tion. Urodynamic studies can clarify the characteristics of M-region stimulation produces a decrease in ure. Damage at the level of cause incontinence is important in both diagnosis the pontine micturition center will produce a loss of and management.

These cir. The PVR ferent fibers from the detrusor muscle to the puden. The dysfunction. Bradley has defined the different neuroanatomic Valsalva maneuver. Laboratory evaluation that starts in the urinary bladder and projects to the includes basic urinalysis to rule out infection.

M region of the pons. An understanding of how these diseases urethral sphincter storage. The lat- wide variety of neurologic diseases including stroke.

The der ultrasound or catheterization is important in the third circuit is a spinal segmental reflex arc with af. Parkinson disease. A normal PVR is less than 50 mL. A detailed history is essential. Figure by Dr. Juan Acosta. This can result in urinary retention. Overflow incontinence is an involuntary loss of genic bladder dysfunctions are listed in Table This is common in mul- compliance. Provides information about bladder an overdistended bladder. It is characterized by overflow inconti- is a spastic bladder.

When the DI at the level of the conus medullaris. Bladder outlet and tant in the evaluation of bladder incontinence. Urodynamic findings in various types of neuro. Symptoms include This classification is based on symptoms.

Sphincter dyssynergia and atonic bladder are common neurogenic causes of elevated PVR. DH is common in patients with nence and increased capacity and compliance. Urodynamics show de- Urge incontinence is an involuntary loss of urine as. These include EMG of Mixed incontinence is a combination of urge and the sphincter and pelvic floor.

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Assesses the integrity of the the urethra and bladder neck. It is usually accompanied by detrusor-sphinc. It can cause increased intra- coureteral reflux. Increased PVR im. Other causes include ence of uninhibited detrusor contractions. Table summarizes treatments for urinary and detrusor-sphincter dyssynergia. Injury to pelvic nerves e. A classic example is diabetic cystopathy. The choice of therapy is based on an understanding of the underlying mechanism of the Spinal Cord Injury dysfunction and therefore the site of the neural Spinal cord injury produces DH.

Following disconnection from the pons. Urologic causes. DH is the most common finding. Some of the dyssynergia. Urodynamic studies show im- effects on the upper urinary tract because voiding is paired detrusor contractility. Pseudodyssynergia occurs as a con- sequence of sphincter bradykinesia. In a clinical study. Urinary sis. New reflexes emerge to drive bladder behavioral techniques that may help with the treat- emptying and cause DH.

During spinal shock. Spinal cord diseases are the most common cause of neurogenic bladder dysfunction.

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The situation is simi- duce an upper motor neuron bladder hyperreflexic lar in other types of neuropathies such as amyloido- and small with urgency and frequency. Lessening of urgency and frequency may last up to 6 months. Oxybutynin Ditropan.

Suprapubic catheterization 3. Detrusor dyssynergia 1. Tolterodine Detrol. Stress incontinence 1. Others include headache. Most frequent side effect: Sacral nerve stimulation bid. Alpha-adrenergic agonist drugs Alpha-adrenergic agonist drugs stimulate a. Tricyclic antidepressants a. Intermittent catheterization 2. Intermittent self-catheterization is perhaps the mainstay of long-term treatment.

Estrogen therapy. The receptors. Anticholinergic agents Tolterodine is tolerated better than spastic bladder a. Intravesical capsaicin Intravesical capsaicin is used for intractable detrusor hyperreflexia.

It has a neurotoxic effect on the afferent C fibers that drive volume-determined reflex detrusor contractions. Estrogen therapy is adjunctive b. Pharmacotherapy is usually not an Bethanechol stimulates cholinergic effective treatment modality. Side effects include bronchospasm. Use only once a day. EMG and so- Erectile dysfunction ED is defined as the persistent matosensory evoked potentials can help in cases of inability to attain or maintain penile erection suffi. Laboratory evaluation The sexual response cycle of excitement.

If drugs are re- fibers that innervate the penis and clitoris. Neurogenic causes include neuropathy. Vascular cient for sexual intercourse. Sleep studies can be coordinated activity of the somatic and autonomic helpful erection usually occurs with each episode of nervous systems innervating the reproductive system.

Many neurogenic dis- The etiology of sexual dysfunction can be multifacto. The sym.. Metabolic and toxic disor- upper urinary tract function and improvement of the ders such as alcohol abuse. Pharmacologic therapy of ED includes selective els of the spinal cord through the hypogastric plexus inhibitors of cGMP-specific phosphodiesterases like and are important in ejaculation.

The sponsible. Chronic illness. As noted previously, lis- a particular letter or belonging to a particular category. Formal testing, however, includes assessing the fluency of spontaneous KEY POINTS speech, the ability to repeat, the ability to comprehend commands, the ability to name both common and less The mental status exam should begin with assess- common objects, and the ability to read and write.

More Language, memory, visuospatial function, neglect, information can be gained by giving longer lists of and tests of frontal lobe function are other key ele- words and charting the patients learning and forget- ments of the mental status exam that can suggest ting curve.

Visual memory can be tested with three focal brain lesions. Patients can be asked to draw a clock, a cube, or another simple figure; alternatively, they can be It is usually easiest to test the cranial nerves or at asked to copy a complex figure drawn by the exam- least to record the results in approximate numerical iner Fig.

Neglect is a mental status finding typically not Olfaction cranial nerve I is rarely tested, but sought by nonneurologists, yet its presence can be a when this is important, each nostril should be tested very important sign. Patients with dense neglect may separately with a nonnoxious stimulus, such as coffee fail to describe items on one side of a picture or of or vanilla. Funduscopic examination is the only Hearing VIII may be evaluated in each ear simply means by which a part of the central nervous system by whispering or rubbing fingers; more detailed assess- the retina can be directly visualized.

Vestibular in three ways: by having the patient pursue a moving function can be tested in many ways, including evalua- target that is a drawing of the letter H in front of tion of eye fixation while the patients head is rapidly their face pursuit , by directing their gaze rapidly to turned or by observation for drift in one direction while various stationary targets saccades , and by fixating the patient is walking in place with the eyes closed.

The presence of nys- should not be hoarse or nasal IX and X. Failure of tagmus should be noted. The gag reflex is also me- strength of jaw opening and palpating over the mas- diated by these nerves. Facial Sternocleidomastoid strength is tested by having sensation can be tested to all modalities over the fore- the patient turn the head against resistance; weakness head V1 , cheek V2 , and jaw V3. The afferent on turning to the left implies a right accessory nerve limb of the corneal reflex is mediated by this nerve.

XI problem. The trapezius muscle is tested by hav- Muscles of facial expression VII are tested by ing the patient shrug their shoulders. If the eyes shut, or show their teeth. Though uncommonly tongue deviates toward the right, the problem lies tested, taste over the anterior two-thirds of the with the right hypoglossal nerve XII.

The presence of fasciculations or of adventitious Cranial nerve testing is most easily performed and movements such as tremor or myoclonus should also recorded in approximate numerical order. Tone is one of the most important parts of the Key elements of the cranial nerve exam include as- sessment of vision and eye movements, facial motor exam.

In the upper extremities, tone is movement and sensation, and movements of the checked by moving the patients arm at the elbow in palate and tongue. Tone in the lower extremities can be tested well only The motor exam includes more than just strength with the patient supine. The examiner lifts the leg up testingin fact, strength should usually be the por- suddenly under the knee; only in the presence of in- tion of the exam performed last.

First, bulk is assessed by observing and palpating Finally, strength or power is assessed, by both func- the muscles and comparing each side to the other and tional observation and direct confrontation Fig. Figure Power testing of individual movements. For each movement, the predominant muscle, peripheral nerve, and nerve root are given.

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Blueprints Pediatrics, 5th Edition. Netter's Neurology, 2nd Edition. Neonatal Neurology Fourth Edition.Giant cell high dose steroids. Georgia Boston. Focal arrhythmic or polymorphic slow activity in the theta or delta range suggests local dys- function in the underlying brain. Students from a wide variety of health care specialties. Charley Mitchell Managing Editor: Evidence-Based Resources. Children present Autosomal recessive cerebellar degenerative with acute onset of limb and gait ataxia as well as disorders dysarthria.