**3. Physical examination**

After performing the primary survey and the clinical interview, the secondary survey can be undertaken. Some manifestations of encephalitis, which may be encountered, are discussed below.

#### **3.1. General observation**

During general observation we can start by assessing the skin. Some etiological agents which can cause encephalitis also cause dermatological lesions. A prime example is the most common viral cause of encephalitis which is HSV, HSV also causes herpetic skin lesions[11], which should been noted and is a good means to reach a fast diagnosis. Other aetiological agents which may also have dermatological signs are EBV[12] in which jaundice and oral petechiae can be observed. A patient infected with WNV occasionally will display a rash[13]. Basciliar angiomatosis[14] a vascular lesion of the skin which can extend to other organs is described as a Chancre and it is a diagnostic sign of primary syphilis. Untreated syphilitic patients can progress to encephalitis and observing skin changes can aid in diagnosis [15]

#### **3.2. Examination of the eye**

Many Etiological agents of Encephalitis can cause ocular symptoms. During a HSV infection the patient can develop keratoconjunctivits[16]. For a patient with an EBV infection a perior‐ bital oedema may be noted[17]. Chorioretinitis[18] is a rare sequelae of West Nile Virus, Being rather uncommon it should still be excluded. Ocular manifestations of Mycoplasma pneumo‐ niae infection other than conjunctivitis are uncommon[19]. The most frequent ocular mani‐ festation of bartonella is neuroretinitis which is usually unilateral[20]. Interstitial keratitis is frequently reported in patients with syphilis[21].

### **3.3. Examination of the oral cavity**

Oral involvement is common in many viral disorders. For example in HSV, ulcers on the buccal mucosa and the tongue are observed[22]. During a bout of EBV infection pharyngitis occurs in 80 - 90% of patients and is usually mild in nature and clears in 7 - 14 days[23]. WNV patients suffer from lymphadenopathy so the tonsils should be examined for any indications of tonsilitis[24]. Oral manifestations of primary syphilis are usually a solitary ulcer on the lip or tongue. Mucous patches and maculopapular lesions are the 2 principal features of secondary syphilis. Gumma formation and syphilitic leukoplakia are the manifestations of tertiary syphilis[25].

their chin on their sternum. Inability to do so is a sign of meningitis. Kerning's sign can also

We move on to a comprehensive assessment of the cranial nerves (table 3).

Optic nerve and oculomotor nerve Pupillary reactions 1 : pages 116-149

Optic nerve Visual acuity, visual fields, ocular fundi1 : page 116

Facial nerve Facial movement, gustation 1 :pages 251-262 Vestibulocochlear nerve Hearing and balance 1 :Pages 263-269

Hypoglossal nerve Tongue protrusion 1 :pages 270 - 276 1. Adapted from: The neurologic examination: Dejong, Russell N. pages 111 to 270

of the nervous system that is responsible for producing the weakness.

Oculomotor nerve, Trochlear nerve, Abducens nerve Extraocular movement, including opening of the eye

Trigeminal nerve Facial sensation, movement of jaw, corneal reflexes 1 :

Glossopharyngeal nerve, Vagus nerve Swallowing, elevation of palate, gag reflex, gustation

Accessory nerve Shrugging shoulders and turning of head 1 :pages 263-269

Now we can assess the motor system to discover if any damage has been done to the motor system. We first start off by testing strength. Strength is tested by having the patient resist your force as you attempt to move their body part against the direction of pull of the muscle that you are evaluating. This is graded on a scale of 0-5, with "0" representing absolutely no visible contraction and "5" being normal[39]. Strength testing is used to decide whether there is a neurogenic weakness and to determine which muscles/movements are affected. In correlation with the remainder of the motor exam, it should be possible to determine the particular part

Testing reflexes is an important part of differentiating whether weakness is of an upper or lower motor neuron type. A reflex can be abolished without damaging motor axons[40]. In the setting of the patient with known weakness, reflex testing is a powerful tool to investigate the cause.[41] Symmetry of the reflexes needs to be considered in determining pathology. Pathological "spread of reflexes" is another objective sign of hyperactivity e.g. sustained clonus. Babinski reflex is a pathological reflex seen in upper motor neuron damage. However the

1 :pages 149-208

pages 208-226

1 :pages 251

Voice and speech 1 :pages 208 - 276

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be performed.

**3.6. Examination of cranial nervs**

Trigeminal nerve , Facial nerve, Vagus nerve ,

**Table 3.** Methods to test cranial nerve function.

Hypoglossal nerve

**3.7. Motor system**

**Cranial nerve Test** Olfactory nerve Smell 1 :page 111

Periauricular lymph nodes are enlarged during West Nile Virus infection[26] Peripheral lymphadenopathy is a manifestation of tuberculosis[27]. Bartonella Henselae, the main causative agent of cat-scratch disease (CSD), appears to be the most common organism responsible for lymphadenopathy in adults and children[28].

#### **3.4. Examination of the abdomen**

After observation now palpations of the abdomen may be undertaken. Mycoplasma is a very rare cause of ascites more commonly cutaneous lesions upon the abdomen should be not‐ ed[29]. Other causes of ascites may be Bartonella Hensele and Syphilis. After general palpation the clinician may want to assess if individual organs can be palpated. Ascites can be evaluated by palpation and percussion. A first clue that there is a possibility of ascites is a rounded symmetrical abdomen with bulging flanks. Undulation test[30] is the gold standard in demonstrating ascites and within this test the clinician should feel for a fluid wave, which would account for a positive test. The clinician may also test to see if there is shifting dullness which is indicative of more than 500ml of ascetic fluid[31].

The clinician should then start with the liver. We position the patient in the recumbent position with the right-handed examiner on the right side of the patient[32]. EBV can cause significant hepatomegaly but it is not as common as splenomegaly[33]. HSV can cause hepatomegaly however it is rare. TB[34] causes hepatomegaly as it infiltrates most organs. Next we can perform the examination of the spleen. We position the patient in the supine position with the knee flexed. We begin below the left costal margin using the right hand firmly pushing down and then releasing[35]. Viral aetiologies in with splenomegaly can occur quite often is an EBV[36] infection. Another viral aetiology of encephalitis is WNV[37] and it is not as common as EBV in causing encephalitis coupled with splenomegaly. A very rare bacterial cause of encephalitis is TB[38], this bacteria infiltrates most organs so splenomegaly should not be ruled out. In order to complete a full physical examination you can perform a renal examination. However common aetiological agents for encephalitis do not usually cause renal disorders.

#### **3.5. Neurological exam**

Next we can perform a thorough neurological exam. This will not only indicate a possibility of encephalitis but also the extent of destruction within the cerebrum. To help differentiate meningitis from encephalitis, we can assess for nuchal rigidity by asking the patient to place their chin on their sternum. Inability to do so is a sign of meningitis. Kerning's sign can also be performed.

#### **3.6. Examination of cranial nervs**

**3.3. Examination of the oral cavity**

**3.4. Examination of the abdomen**

**3.5. Neurological exam**

syphilis[25].

8 Encephalitis

Oral involvement is common in many viral disorders. For example in HSV, ulcers on the buccal mucosa and the tongue are observed[22]. During a bout of EBV infection pharyngitis occurs in 80 - 90% of patients and is usually mild in nature and clears in 7 - 14 days[23]. WNV patients suffer from lymphadenopathy so the tonsils should be examined for any indications of tonsilitis[24]. Oral manifestations of primary syphilis are usually a solitary ulcer on the lip or tongue. Mucous patches and maculopapular lesions are the 2 principal features of secondary syphilis. Gumma formation and syphilitic leukoplakia are the manifestations of tertiary

Periauricular lymph nodes are enlarged during West Nile Virus infection[26] Peripheral lymphadenopathy is a manifestation of tuberculosis[27]. Bartonella Henselae, the main causative agent of cat-scratch disease (CSD), appears to be the most common organism

After observation now palpations of the abdomen may be undertaken. Mycoplasma is a very rare cause of ascites more commonly cutaneous lesions upon the abdomen should be not‐ ed[29]. Other causes of ascites may be Bartonella Hensele and Syphilis. After general palpation the clinician may want to assess if individual organs can be palpated. Ascites can be evaluated by palpation and percussion. A first clue that there is a possibility of ascites is a rounded symmetrical abdomen with bulging flanks. Undulation test[30] is the gold standard in demonstrating ascites and within this test the clinician should feel for a fluid wave, which would account for a positive test. The clinician may also test to see if there is shifting dullness

The clinician should then start with the liver. We position the patient in the recumbent position with the right-handed examiner on the right side of the patient[32]. EBV can cause significant hepatomegaly but it is not as common as splenomegaly[33]. HSV can cause hepatomegaly however it is rare. TB[34] causes hepatomegaly as it infiltrates most organs. Next we can perform the examination of the spleen. We position the patient in the supine position with the knee flexed. We begin below the left costal margin using the right hand firmly pushing down and then releasing[35]. Viral aetiologies in with splenomegaly can occur quite often is an EBV[36] infection. Another viral aetiology of encephalitis is WNV[37] and it is not as common as EBV in causing encephalitis coupled with splenomegaly. A very rare bacterial cause of encephalitis is TB[38], this bacteria infiltrates most organs so splenomegaly should not be ruled out. In order to complete a full physical examination you can perform a renal examination. However common aetiological agents for encephalitis do not usually cause renal disorders.

Next we can perform a thorough neurological exam. This will not only indicate a possibility of encephalitis but also the extent of destruction within the cerebrum. To help differentiate meningitis from encephalitis, we can assess for nuchal rigidity by asking the patient to place

responsible for lymphadenopathy in adults and children[28].

which is indicative of more than 500ml of ascetic fluid[31].

We move on to a comprehensive assessment of the cranial nerves (table 3).


**Table 3.** Methods to test cranial nerve function.

#### **3.7. Motor system**

Now we can assess the motor system to discover if any damage has been done to the motor system. We first start off by testing strength. Strength is tested by having the patient resist your force as you attempt to move their body part against the direction of pull of the muscle that you are evaluating. This is graded on a scale of 0-5, with "0" representing absolutely no visible contraction and "5" being normal[39]. Strength testing is used to decide whether there is a neurogenic weakness and to determine which muscles/movements are affected. In correlation with the remainder of the motor exam, it should be possible to determine the particular part of the nervous system that is responsible for producing the weakness.

Testing reflexes is an important part of differentiating whether weakness is of an upper or lower motor neuron type. A reflex can be abolished without damaging motor axons[40]. In the setting of the patient with known weakness, reflex testing is a powerful tool to investigate the cause.[41] Symmetry of the reflexes needs to be considered in determining pathology. Pathological "spread of reflexes" is another objective sign of hyperactivity e.g. sustained clonus. Babinski reflex is a pathological reflex seen in upper motor neuron damage. However the validity of this reflex clinically argued as changes in foot tapping have been shown to more efficiently show upper motor neuron (UMN) lesions[42].

sensation and if the patient has the capacity to convey the results accurately. Changes in sensation and the symmetry of the changes should be noted. A comprehensive examination

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The principal goal in diagnostics is to identify if the patient is indeed suffering from encepha‐ litis and then the aetiological agent of encephalitis. The most common causes of viral ence‐

EEG changes in encephalopathies are similar to any encephalitis aetiological agent. There is a progressive increase in slow wave activities[47], the degree of which parallels the severity of brain dysfunction. A diffuse slow-wave background followed by the rapid development of periodic complexes in may be diagnostic of herpes-simplex encephalitis[48]. None of these patterns is specific to a particular pathophysiological process or diagnosis, but periodic

MRI is the most sensitive non-invasive test in early diagnosis of HSE due to its high sensitivity to inflammatory increased brain water content. The classical findings in herpes encephalitis are periodic lateral epileptiform discharge and hyper intense T2-weighted signal in the temporal lobe on MRI however these findings are nonspecific[50]. Japanese encephalitis MRI clues would be bilateral thalamic involvement; hemorrhagic involvement can be occasionally seen. Locations in which lesions can be seen are cerebrum, the midbrain and cerebellum, the pons and the basal ganglia. The locations in which hemorrhagic lesions can be seen are cortex, the midbrain, cerebellum, and pontine lesions[51]. Eastern equine encephalitis produces focal radiographic signs what distinguishes it from HSV encephalitis involvement of the basal ganglia and thalami[52]. An MRI preformed on a patient with Epstein-Barr virus encephalitis could show focal lesions in the basal ganglia[53]. The tick-borne encephalitis MRI revealed pronounced signal abnormalities in the basal ganglia and thalamus, without contrast en‐ hancement[54]. Meningovascular syphilis can manifest T2-weighted hyper intense signal

epileptiform discharges are most likely to occur in an acute course of the disease[49].

abnormalities, which are thought to represent cerebral infarctions[55].

trolled bleeding diathesis is also a contraindication.

Lumbar puncture is indicated in a patient with suspected CNS infections (table 5).

Contraindications of lumbar puncture should be kept in mind. If the patient is showing signs of papilledema or an intracranial mass is suspected an urgent CT should be performed[56]. Local skin infections are an absolute contraindication and so are spinal deformities. Uncon‐

phalitis are HSV and VZ encephalitis and they are the only curable causes also.

of the sensory system must be carried out.

**4. Diagnostics**

**4.2. Radiography**

**4.3. Lumbar puncture**

**4.1. EEG**

Muscle bulk can be primarily assessed by inspection. Symmetry is important, with consider‐ ation given to the dominance of the hand and overall body habitus. Generalized wasting or cachexia should be noted and may reflect systemic disease, including neoplasia. Severe atrophy strongly suggests denervation of a muscle, such as with lower motor neuron (LMN) lesions. The most common method is assessing muscle tone is passively moving the patients limb. Tone can either be decreased or increased. The two common patterns of pathologically increased tone, spasticity and rigidity[43]. We should consider the difference between spasticity and rigidity. Spasticity [44] is manifested as an increased resistance to ignition of movement proceeded with a rapid passive movement. Rigidity is an increase in tone which is seen throughout a variety of movements[45].

Coordination is tested as a part of a sequence of movements. Typically the patient is asked to hold his/her hands in front with the palms up, first with the eyes open and then closed (as when examining pronator drift, above). Now we should consider posture, gait and any abnormal movements. The patient should be able to stand erect with eyes open and closed to see if doing so incites abnormality in movements. Then you should ask the patient to walk and assess if there are any abnormalities in gait[46].

Now we can compare the differences between upper motor neurons and lower motor neuron lesion signs (table 4)


1. Adapted from: Reinhard Rohkamm, M.D., Color Atlas of Neurology, 2004 Thieme Pages 46 to 50.

2. Neuroanatomy text and atlas : john H. Martin third edition : 2003 McGraw-Hill

3. Merritt's Neurology 10th Edition (June 2000): by H. Houston Textbook of Neurology Merritt (Editor), Lewis P.

Rowland (Editor), Randy Rowland By Lippincott Williams & Wilkins Publishers

**Table 4.** A comparison between Upper Motor Neurons and Lower Motor Neuron lesion signs

#### **3.8. Sensory system**

Somatic sensation can be tested using the dermatomes. However this is completely subjective to the patient's perception. It is up to the examiner to determine if indeed there is a loss of sensation and if the patient has the capacity to convey the results accurately. Changes in sensation and the symmetry of the changes should be noted. A comprehensive examination of the sensory system must be carried out.
